HydroCurc Specifications.pdf

HydroCurc™
Cambridge Commodities Chemwatch Hazard Alert Code: 2
Part Number: P10489
Version No: 1.1
Safety data sheet according to REACH Regulation (EC) No 1907/2006, as amended by UK REACH Regulations SI 2019/758
Issue Date: 17/03/2021
Print Date: 16/10/2022
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SECTION 1 Identification of the substance / mixture and of the company / undertaking
1.1. Product Identifier
Product name HydroCurc™
Chemical Name Not Applicable
Synonyms Not Available
Chemical formula Not Applicable
Other means of
identification
P10489
1.2. Relevant identified uses of the substance or mixture and uses advised against
Relevant identified uses
The diarylheptanoids are a relatively small class of plant secondary metabolites. They have been reported from plants in 10
different families, e.g. Betulaceae and Zingiberaceae.
The pharmacological activities and mechanisms of action of natural phenylpropanoid glycosides (PPGs) extracted from a variety
of plants such as antitumor, antivirus, anti-inflammation, antibacteria, antiartherosclerosis, anti-platelet-aggregation,
antihypertension, antifatigue, analgesia, hepatoprotection, immunosuppression, protection of sex and learning behavior,
protection of neurodegeneration, reverse transformation of tumor cells, inhibition of telomerase and shortening telomere length in
tumor cells, effects on enzymes and cytokines, antioxidation, free radical scavenging and fast repair of oxidative damaged DNA,
have been reported in the literature.
Phenylpropanoids (PPs) belong to the largest group of secondary metabolites produced by plants, mainly, in response to biotic or
abiotic stresses such as infections, wounding, UV irradiation, exposure to ozone, pollutants, and other hostile environmental
conditions. It is thought that the molecular basis for the protective action of phenylpropanoids in plants is their antioxidant and
free radical scavenging properties. These numerous phenolic compounds are major biologically active components of human
diet, spices, aromas, wines, beer, essential oils,propolis, and traditional medicine.
Phenylpropanoids are ingredients of essential oils including those derived from anis, cinnamon bark, and clove They are often
used for fragrances and aromatherapy. Significant correlation (54-86%) between antiplatelet potency and PPs content in the oils
was found, the key role for this moiety in the control of haemostasis was suggested. As a confirmation of the importance of PP
moieties in defining this kind of biological activity, traditional Chinese medicine preparations, identified as remedies to prevent
blood stasis and thrombus formation were analyzed for their structure/effect relationships. The PPs isoeugenol, ferulic acid,
elemicin, myristicin, ethyl gallate, and dihydroxyacetophenone were recognized as essential platelet protecting compounds.
Many of these substances share both the shikimic acid biosynthetic pathway and a common PP backbone.
It is thought that some beneficial health effects of PPs such as reducing the risk of cancer,osteoporosis and cardiovascular
diseases may depend on their action as estrogen agonists/antagonists via estrogen receptors Estrogen receptor, a nuclear
steroid receptor, binds estrogens and regulates the transcription of estrogen-responsive genes by interacting directly with DNA at
estrogen response elements (ERE) of their promoters.
Product code: P10489 Version No: 1.1 Page 1 of 38

PPs may act as nonsteroidal anti-inflammatory drug (NSAID)-like compounds. The COX-2 gene expression was dramatically
inhibited by the synthesized dimer of ferulic acid.
Phenylpropanoid glycosides (aka phenylethanoid glycosides, PPGs) originate from the shikimic acid-phenylpropanoid pathway
and include simple monosaccharides,consisting of hydroxycinnamic acid and hydroxyphenylethyl (methoxyphenol) moieties
bonded to a central beta-glucopyranose by ester and glycosidic linkages, respectively,and more complex di-and trisaccharides
with one or two additional sugars linked to the core glucose. Members of this compound class have shown a wide range of
biological activity,including inhibition of plant pathogenic bacteria and fungi, antioxidant activity, tumour cell suppression, feeding
stimulation of specialist herbivores and deterrence of generalist insects.
Plant-derived PPGs were found to be effective in the selective inhibition of both tyrosinase activity and melanin synthesis in
cultivated melanocytes without cytotoxic effects.
The PPGs with antioxidant activities, such as acteoside and martynoside, exhibited antiproliferative, cytotoxic, antimetastatic and
immunomodulatory properties
Phenylpropanoids fulfill numerous physiological functions, essential for plant growth and development, as well as plant–
environment interactions. The phenylpropanoid pathway is one of the most frequently investigated metabolic routes, among
secondary metabolite. Phenylpropanoid metabolism generates an enormous array of secondary metabolites, based on the few
intermediates of the shikimate pathway). The shikimate pathway is a source of phenylalanine and the entry point leading to the
biosynthesis of phenylpropanoids. The so-called central phenylpropanoid pathway is defined by three enzymatic activities: (i) the
phenylalanine deamination by phenylalanine ammonia-lyase (PAL) to the trans-cinnamic acid, (ii) the trans-cinnamic acid
hydroxylation to the 4-coumarate, as a resulting from cinnamic acid 4-hydroxylase (C4H) activity, and finally (iii) the 4-coumarate
conversion to the 4-coumaroyl-CoA by 4-coumarate-CoA ligase (4CL).
The cooperating enzymes from the phenylpropanoid pathway were proposed to be organized into complexes called metabolons.
The term “metabolon” encompasses multienzymatic complexes bound to the cellular structural elements – membranes. Most
metabolon models are based on a dynamic, non-covalent aggregation of components on the endoplasmic reticulum (ER)
surface. Organization of enzymes in metabolons is, at the cellular level, a way to optimize biosynthesis. It provides: (i) direct
transport of intermediates between successive enzymes, hence increasing local concentration of the substrate around the
enzyme active center, (ii) minimization of highly biologically active and potentially toxic intermediates within the cell, as well as (iii)
coordination of reactions leading to different branches of pathways with shared enzymes or intermediates. In the
phenylpropanoid pathway, intracellular interactions between biosynthetic enzymes were shown for the central phenylpropanoid
pathway – where PAL and C4H colocalize in the ER. as well as for particular branches leading to the formation of (iso)flavonoids,
monolignols, and anthocyanins.
Antioxidant.
Curcuminoids, the major components of turmeric, are widely used as a traditional medicine and as food additive for their unique
aromatic and coloring properties. Curcuminoids such as curcumin occur in turmeric (Curcuma longa) root and their biological
activities have been extensively investigated, including for their role as nutraceuticals with potential against cancer, diabetes and
inflammation..
Curcuminoids from turmeric and their derivatives have been shown to possess a wide range of biological activities including
antioxidant, anti-inflammatory, anticancer, antimicrobial, neuroprotective, cardioprotective and radioprotective effects.
Two active components of turmeric are the volatile oil and curcuminoids. The essential oils are composed mainly of
sesquiterpenes, many of which are specific for the Curcuma genus. The aroma of this spice is principally derived from a- and
beta-turmerones and aromatic turmerone (Ar-turmerone). The chemical structures of curcuminoids make them much less soluble
in water at acidic and neutral pH, but soluble in methanol, ethanol, dimethyl sulfoxide and acetone. The curcuminoids give a
yellow-orange coloration to turmeric powder due to the wide electronic delocalization inside the molecules that exhibit strong
absorption between 420 to 430 nm in an organic solvent. The curcuminoids are a mixture of curcumin, chemically a
diferuloylmethane mixed with its two derivatives, demethoxycurcumin and bis-demethoxycurcumin
These curcumin derivatives have, like curcumin itself, been tested for their antioxidant activities in vitro. Curcuminoids act as a
superoxide radical scavenger as well as singlet oxygen quencher and gives the antioxidant its effectiveness. The curcuminoids
are capable of inhibiting damage to super coiled plasmid DNA by hydroxyl radicals. It was concluded that the derivatives of
curcumin are good in trapping the 2,2-diphenyl-1-picrylhydrazyl(DPPH) radical as efficiently as curcumin which is a well known
antioxidant
Many curcumin characters are unsuitable for use as drugs by themselves. They have poor solubility in water at acidic and
physiological pH, and also hydrolyze rapidly in alkaline solutions. Therefore, curcumin derivatives are synthesized to increase
their solubility and hence bioavailability.Curcumin derivatives have been synthesized that could possibly be more potent than
curcumin itself. Most common derivatives have different substituents on the phenyl groups. There is an increasing demand of late
for demethoxycurcumin and other curcuminoids because of their biological activity.
Curcuminoids are the promising natural compound with a large variety of therapeutic properties, particularly biological targets
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and interactions, linked to numerous diseases. Unfortunately the clinical applications of curcuminoids are restricted by their poor
solubility, low absorption and bioavailability, high metabolism rate. To overcome these limitations, curcuminoids and their
derivatives have been modified and attached with lipids, micelles, nanoparticles, liposome and metal complexes
Solid lipid nanoparticles preparations have been developed for cosmetics where the curcuminoids are used in cream base. But
there are some stability issues which have not been overcome yet, further studies need to be done to find a suitable formulation
which can be carried out in order to prolong the stability of the curcuminoids.
Turmeric, a spice that has long been recognized for its medicinal properties, has received interest from both the medical/scientific
world and from culinary enthusiasts, as it is the major source of the polyphenol curcumin. It aids in the management of oxidative
and inflammatory conditions, metabolic syndrome, arthritis, anxiety, and hyperlipidemia. It may also help in the management of
exercise-induced inflammation and muscle soreness, thus enhancing recovery and performance in active people. In addition, a
relatively low dose of the complex can provide health benefits for people that do not have diagnosed health conditions. Most of
these benefits can be attributed to its antioxidant and anti-inflammatory effects. Ingesting curcumin by itself does not lead to the
associated health benefits due to its poor bioavailability, which appears to be primarily due to poor absorption, rapid metabolism,
and rapid elimination. There are several components that can increase bioavailability. For example, piperine is the major active
component of black pepper and, when combined in a complex with curcumin, has been shown to increase bioavailability by
2000%. Curcumin combined with enhancing agents provides multiple health benefits.
Curcumin is a bright yellow chemical produced by plants of the Curcuma longa species. It is the principal curcuminoid of turmeric
(Curcuma longa), a member of the ginger family, Zingiberaceae. It is sold as a herbal supplement, cosmetics ingredient, food
flavouring, and food coloring. Chemically, curcumin is a diarylheptanoid, belonging to the group of curcuminoids, which are
phenolic pigments responsible for the yellow color of turmeric.
Curcumin, which shows positive results in most drug discovery assays, is regarded as a false lead that medicinal chemists
include among "pan-assay interference compounds". This attracts undue experimental attention while failing to advance as viable
therapeutic or drug leads although some derivatives of curcumin such as EF-24 have seen a significant amount of research.
Although curcumin has been assessed in numerous laboratory and clinical studies, it has no medical uses established by
well-designed clinical research.. According to a 2017 review of more than 120 studies, curcumin has not been successful in any
clinical trial, leading the authors to conclude that "curcumin is an unstable, reactive, non-bioavailable compound and, therefore, a
highly improbable lead".
Curcumin has been identified by the U.S. Food and Drug Administration as a "fake cancer cure"
Studies have shown that curcumin is a free radical scavenger and hydrogen donor and, depending on the dose and schedule,
can exhibit both pro- and antioxidant activity It also binds to transitional metals like iron and copper and is effective in mitigating
the generation/propagation of free radicals and inflammatory events
Curcumin was found to be stable at high temperatures and in acids, but unstable in alkaline conditions and in the presence of
light.
The intended use of curcumin as a food additive is generally recognized as safe by the U.S. Food and Drug Administration
Curcumin is proposed as a treatment for osteo- and rheumatoid arthritis.
Curcumin is used as an analytical reagent, food dye, biological stain. As an acid-base indicator it is brownish-red with alkalis,
yellow with acids (pH range 7.4-8.4), also an indicator for boron. It Inhibits the induction of nitric oxide synthase in activated
macrophages; inhibits cyclooxygenase and 5-lipoxygenase.
Curcumin activates Nrf2 pathway and suppresses the activation of transcription factor NF-kB. Curcumin induces mitophagy,
autophagy, apoptosis, and cell cycle arrest with antitumor activity. Curcumin reduces renal damage associated with
rhabdomyolysis by decreasing ferroptosis-mediated cell death. Curcumin exhibits anti-infective properties against various human
pathogens like the influenza virus, hepatitis C virus, HIV.
In mouse models, curcumin can reduce Alzheimer’s disease pathology. In vitro studies have shown that curcumin can block
amyloid beta (Abeta) aggregation. Curcumin can cause major structural changes in amyloid aggregates and potentially reduce
Abeta toxicity.
In vitro, curcumin has been shown to inhibit certain epigenetic enzymes (the histone deacetylases: HDAC1, HDAC3, and
HDAC8) and transcriptional co-activator proteins (the p300 histone acetyltransferase). Curcumin also inhibits the arachidonate
5-lipoxygenase enzyme in vitro
Curcumin disrupts cell signal transduction by various mechanisms including inhibition of protein kinase C. These effects may play
a role in the agent's observed antineoplastic properties, which include inhibition of tumour cell proliferation and suppression of
chemically induced carcinogenesis and tumour growth in animal models of cancer.
Curcumin is a potent inhibitor of EGFR tyrosine kinase and IkB kinase. Inhibits inducible nitric oxide synthase (iNOS),
cyclooxygenase and lipoxygenase. It easily penetrates into the cytoplasm of cells, accumulating in membranous structures such
as plasma membrane, endoplasmic reticulum and nuclear envelope.
Curcumin (diferuloylmethane), a natural phenolic compound, is a p300/CREB-binding protein-specific inhibitor of
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acetyltransferase, represses the acetylation of histone/nonhistone proteins and histone acetyltransferase-dependent chromatin
transcription. Curcumin shows inhibitory effects on MAPKs, and has diverse pharmacologic effects including anti-inflammatory,
antioxidant, antiproliferative and antiangiogenic activities. Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine
modification
Therapeutic or pharmacologically-active agent.
An Epidermal Growth Factor Receptor (EGFR) Inhibitor
A substance that blocks the activity of a protein called epidermal growth factor receptor (EGFR). EGFR (aka ErbB1, HER1,
EGFR tyrosine kinase inhibitor, epidermal growth factor receptor inhibitor, and epidermal growth factor receptor tyrosine kinase
inhibitor) is found on the surface of some normal cells and is involved in cell growth. It may also be found at high levels on some
types of cancer cells, which causes these cells to grow and divide. Blocking EGFR may keep cancer cells from growing. Some
EGFR inhibitors are used to treat cancer.
Some patient characteristics, such as never-smoking, female gender, East Asian origin, adenocarcinoma histology, and
bronchioloalveolar subtype, are associated with a greater benefit from treatment with EGFR inhibitors. Studies have identified
gene mutations targeting the kinase domain of the EGFR that are related to the response to inhibitors. Most EGFR mutations
predict a higher benefit from treatment compared with wild-type receptors and are correlated with clinical features related to
better outcome; some EGFR mutations, however, confer drug resistance.
A third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI),is a viable first-line therapy in
non-small cell lung cancer (NSCLC) with sensitizing EGFR mutations
The EGFR is overexpressed, dysregulated or mutated in many epithelial malignancies, and EGFR activation appears important
in tumor growth and progression. Small molecule tyrosine kinase inhibitors (TKIs) target the receptor catalytic domain of EGFR,
Stimulation of Epidermal Growth Factor Receptors (EGFR), found on the cell membrane, may result in tumour growth and
proliferation, inhibition of apoptosis, stimulation of angiogenesis and the promotion of tissue invasion and metastasis. The
receptor is overexpressed in a variety of cancers, including 95% of advanced tumours of the pancreas, up to 90% of tumours in
the kidney and the head and the neck, up to 80% of some lung cancers, and up to 70% and 75% of tumours of the ovaries and
colon respectively.
Ligands such as epidermal growth factor (EGF) and transforming growth factor alpha (TGF alpha) bind to EGFR and turn on a
sequence of signalling pathways important to pro-tumour mechanisms.
Compounds which interfere with the sequence of pro-tumour events that follow the stimulation of EGFR are thought to be useful
as anti-cancer agents. These include monoclonal antibodies directed at this receptor and small molecules targeted at a specific
tyrosine kinase, the enzyme responsible for EGFR phosphorylation and downstream signaling.
Epidermal Growth Factor (EGF) results in cellular proliferation, differentiation, and survival. EGF is a low-molecular-weight
polypeptide first purified from the mouse submandibular gland, but since then found in many human tissues including
submandibular gland, parotid gland. Salivary EGF, which seems also regulated by dietary inorganic iodine, also plays an
important physiological role in the maintenance of oro-oesophageal and gastric tissue integrity. The biological effects of salivary
EGF include healing of oral and gastroesophageal ulcers, inhibition of gastric acid secretion, stimulation of DNA synthesis as well
as mucosal protection from intraluminal injurious factors such as gastric acid, bile acids, pepsin, and trypsin and to physical,
chemical and bacterial agents.
EGF acts by binding with high affinity to epidermal growth factor receptor (EGFR) on the cell surface and stimulating the intrinsic
protein-tyrosine kinase activity of the receptor. The tyrosine kinase activity, in turn, initiates a signal transduction cascade that
results in a variety of biochemical changes within the cell - a rise in intracellular calcium levels, increased glycolysis and protein
synthesis, and increases in the expression of certain genes including the gene for EGFR - that ultimately lead to DNA synthesis
and cell proliferation.
Tyrosine kinase inhibitors (TKIs or tyrophostins - short name "nibs") are pharmaceutical drugs that inhibits tyrosine kinases.
Tyrosine kinases are enzymes responsible for the activation of many proteins by signal transduction cascades. The proteins are
activated by adding a phosphate group to the protein (phosphorylation), a step that TKIs inhibit. TKIs are typically used as
anticancer drugs.
Tyrosine kinases are divided into two groups; receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (nRTKs).
Receptors are generally embedded in cell membranes and have both an intra- and extracellular component.
Unlike RTKs, nRTKs lack receptor-like features such as an extracellular ligand-binding domain and a transmembrane-spanning
region. Most of the nRTKs are localized in the cytoplasm but some nRTKs are anchored to the cell membrane through amino-
terminal modification. The most common theme in nRTKs and RTK regulation is tyrosine phosphorylation
Receptor tyrosine kinase inhibitors (RTKIs) are bioactive, usually aromatic, small molecules that are desirable drug targets as
therapy for cancer, inflammatory, metabolic, proliferative and neurodegenerative diseases. Receptor tyrosine kinase inhibitors
can bind to the active site of a RTK thus preventing phosphorylation and by doing so inhibit, regulate or modulate signaling, often
with cytostatic activity. Some potent kinase inhibitors will exhibit selectivity for a certain RTK, while others are less selective. For
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example, some tyrphostins are potent and selective inhibitors of Vascular Endothelial Growth Factor Receptor (VEGFR) receptor
kinases, but weak inhibitors of Platelet Derived Growth Factor Receptor (PDGFR) tyrosine kinases and Epidermal Growth Factor
Receptor (EGFR) tyrosine kinases.
Non-receptor tyrosine kinase (nRTK) inhibitors block intracellular processes involved in the tumor transformation of cells and / or
maintenance of malignant phenotype of tumor cells. The pathologically increased activity of nRTK may be responsible for growth
and progression of cancer cells, the induction of drug-resistance, formation of metastasis and tumor neovascularization.
There are three main sub-classes of kinases, Src, Tec and Syk kinases, that are intimately implicated in TCR (T cell antigen
receptors) signaling, a foremost step in cellular recognition of attacking pathogens and tissue damage. The over-activation of
these tyrosine kinases causes a change in gene expression of the affected cells. The most affected genes are of cytokines that
coordinate the duration as well as extent of inflammation. The tyrosine kinases are also involved in functioning and signaling of
various inflammatory cytokines such as TNF-alpha, IL-2 and IL-6
The process of tumourigenesis frequently involves protein kinase activation events, which can result from either mutations, or
chromosomal rearrangements. Gene rearrangements, leading to the expression of constitutively activated fusion tyrosine kinase
receptors, have been increasingly identified as a common feature of malignancies.
The expression of such gene fusions in a tumor can create a phenomenon termed ‘oncogene addiction in which the tumor
becomes dependent on signaling by the aberrant kinase pathway, thus rendering its survival and continued proliferation
exquisitely sensitive to targeted inhibition with small molecule tyrosine kinase inhibitor drugs. Expression of the proteins encoded
by these tyrosine kinase fusion genes can, in most cases, be shown to function independently as oncogenic drivers, capable of
activating critical downstream pathways involved in the malignant phenotype, resulting in transformation of cells in vitro. Some of
the most important kinases that have been shown to undergo rearrangement in human cancers include the anaplastic lymphoma
kinase (ALK), ROS1 kinase, and the neurotrophic receptor tyrosine kinases (NTRKs).
TKIs operate by four different mechanisms: they can compete with adenosine triphosphate (ATP), the phosphorylating entity, the
substrate or both or can act in an allosteric fashion, namely bind to a site outside the active site, affecting its activity by a
conformational change.TKIs have been shown to deprive tyrosine kinases of access to the Cdc37-Hsp90 molecular chaperone
system on which they depend for their cellular stability, leading to their ubiquitylation and degradation. Signal transduction
therapy can in principle also apply for non-cancer proliferative diseases and for inflammatory conditions.
Differences in the amino acids present at the active binding sites for the various protein kinases allowed for TKIs that target
selective tyrosine kinases to be developed.3 Some of the different types of TKIs are explained below
BCR-ABL kinase inhibitors ABL is a type of tyrosine kinase, but a mutation can produce BCR-ABL, which is a hybrid form of
the kinase. BCR-ABL is constitutively active (i.e. constantly active despite regulation or feedback) compared to ABL. BCR-ABL is
active in certain types of cancer cells, and this deregulated activity can lead to malignancy, e.g. chronic myelogenous leukemia.
Epidermal growth factor receptor inhibitors: Epidermal growth factor (EGFR) is also known as ErbB1 or HER1,is required for
epithelial cell growth and differentiation.
Inhibitors of angiogenesis: Vascular endothelial growth factor (VEGF) is well studied for its angiogenic effects (creation of new
blood vessels) in cancer cells.2 When VEGF binds to a VEGFR, activation of VEGFR tyrosine kinase starts off the pathways of
mitosis and anti-apoptotic signalling in the endothelial cells (apoptosis being programmed cell death).
Janus kinase inhibitors are orally delivered small molecules that target cytokine signalling by preventing phosphorylation of
Janus kinases associated with the cytokine receptor. Subsequently, phosphorylation of signal transducers and activators of
transcription that relay Janus kinase signalling and transcription of cytokines in the nucleus will be diminished. Key cytokines in
the pathogenesis of inflammatory bowel diseases are targeted by Janus kinase inhibitors. Several Janus kinase inhibitors are in
development for the treatment of inflammatory bowel diseases.
A histone deacetylase inhibitor (HDAC inhibitor/ HDI)
Histone deacetylase inhibitors (HDAC inhibitor/ HDIs) have a long history of use in psychiatry and neurology as mood stabilisers
and anti-epileptics. HDIs are being studied as a mitigator for neurodegenerative diseases..The prime example of an HDI is
valproic acid. HDAC inhibitors have been reported to produce antidepressant and pro-cognitive effects in animal models.
There has been an effort to develop HDIs as a cancer treatment or adjunct The exact mechanisms by which the compounds may
work are unclear, but epigenetic pathways are proposed.
HDACs cause post-translational acetylation of core nucleosomal histones, which affects chromatin structure and thus regulates
gene expression including those important for cell survival, proliferation, differentiation and apoptosis [15]. HDACs also act as
members of a protein complex which recruits transcription factors to the promoter region of genes and regulate cell cycle
regulatory protein acetylation status . As high HDAC expression and histone hypoacetylation have been noted in cancer in the
setting of transcriptional repression of genes, the HDAC inhibitors have been investigated as therapeutic agents in cancer
By modulating the acetylation of both histone and nonhistone substrates, HDAC inhibitors can regulate a variety of cell functions
through indirect effects on downstream targets. Importantly, many of these targets are key regulators of receptor tyrosine kinase (
RTK) signaling pathways. Several studies also suggest a synergy between RTK or conventional chemotherapeutics and HDAC
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inhibition in cancer cells
HDIs should not be considered to act solely as enzyme inhibitors of HDACs. A large variety of nonhistone transcription factors
and transcriptional co-regulators are known to be modified by acetylation. HDIs can alter the degree of acetylation nonhistone
effector molecules and thereby increase or repress the transcription of genes by this mechanism.
In more recent times, HDIs are being studied as a mitigator for neurodegenerative diseases such as Alzheimer's disease and
Huntington's disease. Enhancement of memory formation is increased in mice given the HDIs sodium butyrate or SAHA, or by
genetic knockout of the HDAC2 gene in mice. While that may have relevance to Alzheimer's disease, it was shown that some
cognitive deficits were restored in actual transgenic mice that have a model of Alzheimer's disease (3xTg-AD) by orally
administered nicotinamide, a competitive HDI of Class III sirtuins
Posttranslational modifications regulate the activity, stability, and localization of proteins that can confer both positive and
negative regulation to diverse biological systems. Acetylation is a protein modification that regulates eukaryotic gene expression.
The addition of acetyl groups to nuclear proteins (such as histones and transcription factors) by histone acetyltransferase
enzymes is frequently associated with activation of gene expression, whereas removal of acetyl groups by deacetylase enzymes
is commonly associated with transcriptional repression.
Histone deacetylases (HDACs) function in a wide range of molecular processes, including gene expression, and are of significant
interest as therapeutic targets. Although their native complexes, subcellular localization, and recruitment mechanisms to
chromatin have been extensively studied, much less is known about whether the enzymatic activity of non-sirtuin HDACs can be
regulated by natural metabolites. Several coenzyme A (CoA) derivatives, such as acetyl-CoA, butyryl-CoA, HMG-CoA, and
malonyl-CoA, as well as NADPH but not NADP+, NADH, or NAD+, act as allosteric activators of recombinant HDAC1 and
HDAC2 in vitro following a mixed activation kinetic. In contrast, free CoA, like unconjugated butyrate, inhibits HDAC activity in
vitro. Analysis of a large number of engineered HDAC1 mutants suggests that the HDAC activity can potentially be decoupled
from “activatability” by the CoA derivatives. In vivo, pharmacological inhibition of glucose-6-phosphate dehydrogenase (G6PD) to
decrease NADPH levels led to significant increases in global levels of histone H3 and H4 acetylation. The similarity in structures
of the identified metabolites and the exquisite selectivity of NADPH over NADP+, NADH, and NAD+ as an HDAC activator reveal
a previously unrecognized biochemical feature of the HDAC proteins with important consequences for regulation of histone
acetylation as well as the development of more specific and potent HDAC inhibitors.
HDACs catalyze the removal of acetyl groups from lysine residues of a wide array of substrate proteins in addition to histones,
including transcription factors and other nuclear and cytoplasmic proteins. Based on phylogenetic sequence analysis, HDACs are
classified into class I (HDAC1-3 and -8), class II (HDAC4-7 and -9), class III, also known as sirtuins (SIRT1-7), and class IV
(HDAC11).
While class I HDACs are localized predominantly within the nucleus, class II HDACs shuttle into and out of the nucleus in
response to intracellular signaling. Class IIa HDACs, which include HDAC4, 5, 7, and 9, commonly act as transcriptional
corepressors and play diverse roles in cell biology. They interact with MEF2 transcription factors and the N-CoR, BCoR, and
CtBP corepressors. Class IIa HDACs found in a wide variety of biological processes. They play key roles in activity-dependent
gene regulation. They respond to neural activity both in the CNS, heart, and at the neuromuscular junction. In addition, the
therapeutic potential of HDAC4 inhibition is a therapeutic strategy to combat diverse indications. They include inflammatory
hyperalgesia cardiac hypertrophy, certain cancers, muscle-wasting disorders. It also has therapeutic potential in progressive
neurodegenerative disease
Class I HDACs 1-3 are critical for activating androgen receptor (AR)-mediated transcription. AR is an androgen-activated
transcription factor and drives prostate cancer (PCa) progression. Thus, targeting these HDACs is a promising strategy for
treating PCa. Entinostat, an aminobenzamide analog specific to HDACs 1-3, extended overall survival for patients with breast
cancer resistant to endocrine therapy. These observations suggest that HDACi selective to HDACs 1-3 may be effective for
treating solid tumors including PCa.
HDACs are ubiquitously expressed and play roles in regulation of cell growth, differentiation, and death . They show deregulated
expression in pathological states such as cancer and have therefore garnered significant interest as therapeutic targets . There
are currently many clinical trials underway to determine the therapeutic efficacies of several HDAC inhibitors that have shown
anti-neoplastic functions in cell culture and animal studies. Two HDAC inhibitors, Vorinostat and Romidepsin, have been
approved for use in treatment of cutaneous T-cell lymphoma . Other HDAC inhibitors have been used successfully as mood
stabilizers and anti-epileptics and have shown promise in treatment of diverse neurological diseases such as Huntington and
Alzheimer disease, amyotrophic lateral sclerosis (ALS), and spinal muscular atrophy.
HDACs are generally found in multiprotein complexes, the functions of which can be regulated through several mechanisms.
These complexes can be recruited to specific genomic loci by DNA-binding proteins, thereby bringing HDACs to close proximity
of their histone substrates. HDAC-containing complexes are localized in both the nucleus and cytoplasm but can shuttle
between the two subcellular compartments, affecting their accessibility to relevant substrates . Modulating the stability of
interactions between HDACs and other members of the complexes in which they reside can also affect the overall activity of
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HDAC complexes .
Other regulatory mechanisms may affect the HDAC enzymatic activity more directly. Acetylation of HDAC1 protein reduces its
enzymatic activity both in vivo and in vitro . Sumoylation of HDAC1 increases its enzymatic activity, and phosphorylation of
HDAC1 stimulates both its activity and complex formation. The catalytic activity of class III HDACs (Sirtuins) depends on the
presence of the oxidized form of nicotinamide adenosine dinucleotide (NAD+). Because the availability of NAD+ is linked to
cellular metabolism, the metabolic state of the cell could be a direct regulator of sirtuins). Such direct regulation by a metabolic
cofactor may transmit information on the cellular energy state to the chromosome, influencing nuclear functions such as gene
expression and DNA replication
Histones are highly conserved proteins that play important roles, not only in compacting DNA in the cell, but which also have
dynamic functions in many physiological and molecular processes. Covalent modifications of the histone tail, in particular on
lysine residues, are an essential part of epigenetic mechanisms to regulate processes like DNA repair and gene transcription The
complex code of histone tail modifications is tightly regulated and includes a variety of modifications, most prominently
acetylation and methylation of lysine and arginine residues. Enzymes that modify or bind to these residues have been implicated
in a variety of diseases including cancer, inflammatory diseases, heart disease and neurodegenerative diseases Methylation of
histone lysines was once thought by many to be irreversible, but two classes of histone lysine demethylases (KDMs) have now
been identified that catalyse the removal of these methylation marks
Histones constitute the basic scaffold proteins around which DNA is wound to form nucleosomes which are packed into higher
order structures to form chromatin. Methylated lysine and arginine residues on histone tails are believed to be regulatory
hallmarks for discriminating transcriptionally active and inactive chromatin
Histone is an integral part of the nucleosome, the basic unit of chromatin The nucleosome core particle consists of ~147 base
pairs of DNA wrapped around the histone octamer (H2A, H2B, H3 and H4) in two circles. The core particles of the nucleosome
are connected to histone H1 via ~60 base pairs of connective DNA. The N-terminal ‘tail’ of the histones is an important target for
several histone-modifying enzymes
Histone methylation and demethylation are an important pair of histone epigenetic modifications, which play key roles in gene
transcription regulation. Methylation occurs on the lysine and arginine residues of histones, including K9, K27 and K36 of histone
H3, K20 of H4, R2, R17 of H3, and R3 of H4. The transcriptional regulation of histone lysine methylation is closely associated
with lysine residue sites and methylation degree. The methylation of H3K4, H3K36 and H3K79 is often accompanied by the
activation of gene transcription, while the methylation of H3K9, H3K27 and H4K20 inhibits gene transcription
A code has been developed to indicate the substrate for a histone modifying enzymes. The substrate is first specified by the
histone subunit (H1, H2A, H2B, H3, H4) and then the one letter designation and number of the amino acid that is methylated.
Lastly, the level of methylation is sometimes noted by the addition of "me#", with the numbers being 1, 2, and 3 for
monomethylated, dimethylated, and trimethylated substrates, respectively. For example, H3K9me2 is histone H3 with a
dimethylated lysine in the ninth position.
IKK inhibitor (syn: inhibitory kappa B kinase inhibitor NF-kB kinase inhibitor)
The IKKs generally serve to transduce pro-inflammatory and growth stimulating signals that contribute to major cellular
processes but also play a key role in the pathogenesis of a number of human diseases. Therefore, the catalytic IKKs represent
attractive targets for intervention with small molecule kinase inhibitors.
A number of adenosine triphosphate (ATP)-competitive IKKbeta-selective inhibitors have been developed but have demonstrated
a lack of activity against IKK alpha. A number of these chemicals have also exhibited detrimental outcomes such as cellular
toxicity and immuno-suppression
NF-kB, which is activated by IKK, is involved in the progression of inflammatory disease. The well-recognized role of NF-kB in
underpinning cellular inflammation has implicated the IKKs as important intermediates involved in a number of disease conditions
including asthma, atherosclerosis, neurodegeneration, rheumatoid arthritis (RA) and inflammatory bowel disease (IBD) . Ideally,
the inhibition of NF-?B would therefore be a worthwhile therapeutic strategy; unfortunately, however, there are caveats. NF-kB
proteins play a pivotal role in normal physiological functions such as innate immunity and cell survival.
The transcription factors NF-kB and IFN control important signaling cascades and mediate the expression of a number of
important pro-inflammatory cytokines, adhesion molecules, growth factors and anti-apoptotic survival proteins. IkB kinase (IKK)
and IKK-related kinases (IKKepsilon and TBK1) are key regulators of these biological pathways and, as such, modulators of
these enzymes may be useful in the treatment of inflammatory diseases and cancer.
Inhibition of IkB kinase (IKK) and IKK-related kinases, IKBKE (IKK epsilon) and TANK-binding kinase 1 (TBK1), has been
investigated as a therapeutic option for the treatment of inflammatory diseases and cancer
Though functionally adaptive in response to inflammatory stimuli, deregulation of NF-kB signaling has been exploited in various
disease states. Increased NF-kB activity as a result of constitutive IKK-mediated phosphorylation of IkB-alpha has been observed
in the development of atherosclerosis, asthma, rheumatoid arthritis, inflammatory bowel diseases, and multiple sclerosis.
Specifically, constitutive NF-kB activity promotes continuous inflammatory signaling at the molecular level that translates to
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chronic inflammation phenotypically. Furthermore, the ability of NF-kB to simultaneously suppress apoptosis and promote
continuous lymphocyte growth and proliferation explains its intimate connection with many types of cancer.
IKK (IkB kinase) is an enzyme complex that is involved in propagating the cellular response to inflammation. An IkB kinase is an
enzyme that catalyzes the chemical reaction: ATP + IkB protein ADP + IkB phosphoprotein. The IkB kinase enzyme complex is
part of the upstream NFkB signal transduction cascade. The IkBalpha (inhibitor of kappa B) protein inactivates the NF-kB
transcription factor by masking the nuclear localization signals of NF-kB proteins and keeping them sequestered in an inactive
state in the cytoplasm. IKK specifically, phosphorylates the inhibitory IkBalpha protein. This phosphorylation results in the
dissociation of IkBa from NF-kB. NF-kB, which is free, migrates into the nucleus and activates the expression of at least 150
genes; some of which are anti-apoptotic. IKK belongs to the family of transferases, specifically those transferring a phosphate
group to the sidechain oxygen atom of serine or threonine residues in proteins.
IkB kinase activity is essential for activation of members of the nuclear factor-kB (NF-kB) family of transcription factors, which
play a fundamental role in lymphocyte immunoregulation. Activation of the canonical, or classical, NFkB pathway begins in
response to stimulation by various pro-inflammatory stimuli, including lipopolysaccharide (LPS) expressed on the surface of
pathogens, or the release of pro-inflammatory cytokines such as tumor necrosis factor (TNF) or interleukin-1 (IL-1). Following
immune cell stimulation, a signal transduction cascade leads to the activation of the IKK complex, an event characterized by the
binding of NEMO (NF-kappa-B essential modulator) to the homologous kinase subunits IKK-a and IKK-beta. The IKK complex
phosphorylates serine residues (S32 and S36) within the amino-terminal domain of inhibitor of NF-kB (IkB-alpha) upon activation,
consequently leading to its ubiquitination and subsequent degradation by the proteasome. Degradation of IkB-alpha releases the
prototypical p50-p65 dimer for translocation to the nucleus, where it binds to kB sites and directs NF-kB-dependent
transcriptional activity NF-kB target genes can be differentiated by their different functional roles within lymphocyte
immunoregulation and include positive cell-cycle regulators, anti-apoptotic and survival factors, and pro-inflammatory genes.
Collectively, activation of these immunoregulatory factors promotes lymphocyte proliferation, differentiation, growth, and survival
A leukotriene receptor antagonist (leukast) or leukotriene synthesis inhibitor:
An antileukotriene, also known as leukotriene modifier and leukotriene-receptor antagonist, is a medication which functions as a
leukotriene-related enzyme inhibitor (arachidonate 5-lipoxygenase , 5-LOX) or leukotriene receptor antagonist (cysteinyl
leukotriene receptors) and consequently opposes the function of these inflammatory mediators; leukotrienes are produced by the
immune system and serve to promote bronchoconstriction, inflammation, microvascular permeability, and mucus secretion in
asthma and chronic obstructive pulmonary disease (COPD). Leukotriene receptor antagonists are sometimes colloquially
referred to as leukasts.
The production of leukotrienes is usually accompanied by the production of histamine and prostaglandins, which also act as
inflammatory mediators.
Both leukotriene synthesis inhibitors and leukotriene receptor antagonists have been suggested to induce beneficial effects at
different stages of the atherosclerosis process. Leukotriene inhibition is of particular interest in the context of diseases associated
with an increased cardiovascular risk, such as COPD and periodontitis .
Leukotrienes are important mediators of immune and inflammatory responses, especially in asthma and allergies, and may also
play a role in arthritis, cardiovascular and other diseases.
Leukotrienes are so named due to their source from leukocytes and the presence of three conjugated double bonds in their
structure. They are often produced in response to an allergen, and generally with histamine. They act locally, as autocrine or
paracrine signalers. Leukotrienes are divided into two classes - leukotriene B4 (highly potent inflammatory) and cysteinyl-
substituted (sulfidopeptide Leukotrienes that contain a cysteinyl molecule (cysteinyl leukotrienes) cause constriction of smooth
muscle in the airway wall; swelling, edema, and leakage from blood vessels in the airway walls; mucus gland stimulation; and
secretion of mucus. They also attract eosinophils into the airways.
Leukotrienes are a subset of eicosanoids, each containing 20 carbons and a carboxylic acid moiety.
There are two main approaches to block the actions of leukotrienes; antagonism and inhibition.
· Antagonism of cysteinyl-leukotriene type 1 receptors (LTRAs): Agents block the actions of cysteinyl leukotrienes at the CysLT1
receptor on target cells such as bronchial smooth muscle via receptor antagonism. These modifiers have been shown to improve
asthma symptoms, reduce asthma exacerbations and limit markers of inflammation such as eosinophil counts in the peripheral
blood and bronchoalveolar lavage fluid. This demonstrates that they have anti-inflammatory properties
· Drugs that inhibit the enzyme 5-lipoxygenase will inhibit the synthetic pathway of leukotriene metabolism; drugs block the
5-lipoxygenase activating protein (FLAP) inhibit functioning of 5-lipoxygenase and may help in treating atherosclerosis. Some
chemicals found in trace amounts in food, and some dietary supplements, also have been shown to inhibit 5-LOX, such as
baicalein caffeic acid, curcumin, hyperforin and St John's wort
Leukotriene Receptors (cys-LTs) are a family of potent bioactive lipids that act through two structurally divergent G protein-
coupled receptors, termed the CysLT1 and CysLT2 receptors. The cysteinyl leukotrienes LTC4, LTD4, and LTE4 are important
mediators of human bronchial asthma. Leukotriene Receptor is a member of the superfamily of G protein-coupled receptors and
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uses a phosphatidylinositol-calcium second messenger system. Activation of CysLT1 by LTD4 results in contraction and
proliferation of smooth muscle, oedema, eosinophil migration and damage to the mucus layer in the lung. Leukotriene receptor
antagonists, called LTRAs for short, are a class of oral medication that is non-steroidal. They may also be referred to as
anti-inflammatory bronchoconstriction preventors. LTRAs work by blocking a chemical reaction that can lead to inflammation in
the airway
The cysteinyl leukotrienes (CysLTs), LTC4, LTD4, and LTE4, mediate their actions through two distinct G-protein coupled
receptors. LTD4 is the preferred ligand for the CysLT1 receptor, whereas LTC4 and LTD4 bind with approximately equal affinity to
the CysLT2 receptor
Lipoxygenase (LOX, lipoxidase) inhibitor:
LOXs belong to a heterogenous family of lipid-peroxidising enzymes and are involved in the biosynthesis of mediators of
inflammation.
Studies have shown that LOX enzymatic activity can be inhibited by phenolic antioxidants such as nordihydroguaiaretic acid and
caffeic acid, suggesting a beneficial role of dietary polyphenol intake.
LOXs are dioxygenases that catalyze the formation of corresponding hydroperoxides from polyunsaturated fatty acids such as
linoleic acid and arachidonic acid. LOX enzymes are expressed in immune, epithelial, and tumor cells that display a variety of
physiological functions, including inflammation, skin disorder, and tumorigenesis.
The oxygenated lipids initiate subsequent biological reactions, activate cellular signaling mechanisms through specific cell
surface receptors, or are further metabolized into potent lipid mediators.
The lipoxygenase pathway is active in leukocytes and other immunocompetent cells, including mast cells, eosinophils,
neutrophils, monocytes, and basophils. When such cells are activated, arachidonic acid is liberated from cell membrane
phospholipids by phospholipase A2, and donated by the 5-lipoxygenase-activating protein (FLAP) to 5-lipoxygenase. FLAP
convert arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which spontaneously reduces to
5-hydroxyeicosatetraenoic acid (5-HETE). 5-HETE is converted 5-lipoxygenase into leukotriene A4 (LTA4) which are further
metabolised to the more stable 5-oxo-ETE series, all of which have pro-inflammatory actions.
In the humans and mice, six LOX isoforms have been known.
· 5-LOX is a distinct isoform playing an important role in asthma and inflammation. 5-LOX and its derivatives are highly
expressed within human carotid, aortic, and coronary artery plaques. So-called leukotrienes are produced by 5-LOX interactions
with arachidonic acid. This isoform causes the constriction of bronchioles in response to cysteinyl leukotrienes such as LTC4,
thus leading to asthma. It also induces neutrophilic inflammation by its recruitment in response to LTB4. Importantly, 5-LOX
activity is strictly regulated by 5-LOX activating protein (FLAP) though the distribution of 5-LOX in the nucleus. FLAP inhibitors
essentially modulate the transportation of 5-LOX from the nucleus to the cytoplasm, leading to suppressive
5-hydroperoxyeicosatetraenoic acid (5-HPETE) production. This mode of action of 5-LOX inhibitor is unique, and there are no
similar regulatory mechanisms and drugs for other LOX isoforms.
· 12-LOX is an isoform expressed in epithelial cells and myeloid cells including platelets. Many mutations in this isoform are
found in epithelial cancers, suggesting a potential link between 12-LOX and tumorigenesis. 12R-LOX can be found in the
epithelial cells of the skin. Defects in this gene result in ichthyosis, a cutaneous disorder characterized by pathophysiologically
dried skin due to abnormal loss of water from its epithelial cell layer. Similarly, eLOX-3, which is also expressed in the skin
epithelial cells acting downstream 12R-LOX, is another causative factor for ichthyosis. Genetic studies have suggested that
ALOX12 gene polymorphisms are associated with cancers , neurological disorders, hypertension, fat mass, and bone mineral
density
· 15-LOX, a prototypical enzyme originally found in reticulocytes, in macrophages and other immune cells as well as epithelial
cells 15-OX-2, which is expressed in epithelial cells and leukocytes, has different substrate specificity in the humans and mice,
therefore, the role of them in mammals has not been established. production. 15-LOX has been hypothesized to initiate and/or
promote atherosclerosis through low density lipoprotein (LDL) oxidation. This is based on the “oxidative LDL theory” that
oxidation of lipids induces atherosclerosis and its inhibition by antioxidants prevents atherogenesis.
There is a general acceptance that cyclooxygenase (COX) inhibitor non-steroidal anti-inflammatory drugs (NSAIDs) induce colon
cancer in humans. One suggested reason is that the balance between COX and LOX determines tumorigenesis critically. Under
low COX activity, arachidonic acid released from cell membranes in response to external stimuli is preferentially metabolized by
LOX enzymes. There is evidence that a 15-LOX metabolite 13S-HPODE (13S-hydroperoxyoctadecaenoic acid) generated from
linoleic acid induces apoptosis in colon cancer.
While the overall structure of mammalian LOX enzymes seems to be similar, each isoform has unique properties, such as
substrate specificity. In most cases, the structure depends on the shape of the substrate cavity and the coordination of histidine
residues or alternatives to a non-heme iron atom at the catalytic center. Importantly, LOX enzymes require a lag period for the
activation of enzymes from an inactive ferrous form to an active ferric form by either molecular oxygen or lipid hydroperoxides.
Enzymatic activity is also regulated by the N-terminal beta-barrel region of polypeptides, where this region has a similar amino
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acid sequence to the C2-like domain; thus, Ca2+-mediated activation via interaction with the plasma membrane has been
proposed.
Reagent.
Nitric oxide inhibitor.
Nitric Oxide Synthase (NOS) exists in three distinctly different structural isoforms namely neuronal (nNOS), endothelial (eNOS)
and inducible (iNOS). Nitric oxide (NO), which is a molecular messenger and is synthesized by nitric oxide synthase (NOS) from
L-arginine and molecular oxygen, is responsible for a number of pathological and physiological processes in mammalians. As
NOS isozymes are involved in different aspects of signal transduction, NOS inhibitors have found importance in managing
hypotensive effects of drugs, ischemic reperfusion injury and inflammatory response to cytokines. Thereby NOS inhibitors are
novel therapeutic approach towards various diseases, and can also be used in investigating other biological functions of NO.
Some polyketides show physiologic activities towards plants, such as phytoalexins, with the budding of seeds and adjusting of
growth. Most polyketides have phenolic hydroxy groups and show antioxidative activity.
Uses advised against Not Applicable
1.3. Details of the manufacturer or supplier of the safety data sheet
Registered company name Cambridge Commodities
Address Lancaster Way Business Park, Ely, Cambridgeshire Cambridgeshire CB6 3NX United Kingdom
Telephone +44 1353 667258
Fax Not Available
Website
Email Info@c-c-l.com
1.4. Emergency telephone number
Association / Organisation Not Available
Emergency telephone
numbers
Not Available
Other emergency
telephone numbers
Not Available
SECTION 2 Hazards identification
2.1. Classification of the substance or mixture
Classified according to
GB-CLP Regulation, UK SI
2019/720 and UK SI
2020/1567 [1]
H335 - Specific Target Organ Toxicity - Single Exposure (Respiratory Tract Irritation) Category 3, H315 - Skin Corrosion/Irritation
Category 2, H319 - Serious Eye Damage/Eye Irritation Category 2, H360Fd - Reproductive Toxicity Category 1B
Legend: 1. Classified by Chemwatch; 2. Classification drawn from GB-CLP Regulation, UK SI 2019/720 and UK SI 2020/1567
2.2. Label elements
Hazard pictogram(s)
Not Available
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Signal word Danger
Hazard statement(s)
H335 May cause respiratory irritation.
H315 Causes skin irritation.
H319 Causes serious eye irritation.
H360Fd May damage fertility. Suspected of damaging the unborn child.
Supplementary statement(s)
Not Applicable
Precautionary statement(s) Prevention
P201 Obtain special instructions before use.
P271 Use only outdoors or in a well-ventilated area.
P280 Wear protective gloves, protective clothing, eye protection and face protection.
P261 Avoid breathing dust/fumes.
P264 Wash all exposed external body areas thoroughly after handling.
Precautionary statement(s) Response
P308+P313 IF exposed or concerned: Get medical advice/ attention.
P305+P351+P338 IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continue rinsing.
P312 Call a POISON CENTER/doctor/physician/first aider/if you feel unwell.
P337+P313 If eye irritation persists: Get medical advice/attention.
P302+P352 IF ON SKIN: Wash with plenty of water.
P304+P340 IF INHALED: Remove person to fresh air and keep comfortable for breathing.
P332+P313 If skin irritation occurs: Get medical advice/attention.
P362+P364 Take off contaminated clothing and wash it before reuse.
Precautionary statement(s) Storage
P405 Store locked up.
P403+P233 Store in a well-ventilated place. Keep container tightly closed.
Precautionary statement(s) Disposal
P501 Dispose of contents/container to authorised hazardous or special waste collection point in accordance with any local regulation.
2.3. Other hazards
Ingestion may produce health damage*.
Cumulative effects may result following exposure*.
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Limited evidence of a carcinogenic effect*.
REACH - Art.57-59: The mixture does not contain Substances of Very High Concern (SVHC) at the SDS print date.
SECTION 3 Composition / information on ingredients
3.1.Substances
See 'Composition on ingredients' in Section 3.2
3.2.Mixtures
1.CAS No
2.EC No
3.Index No
4.REACH No
%[weight] Name
Classified according to GB-CLP Regulation, UK SI
2019/720 and UK SI 2020/1567
SCL /
M-Factor
Nanoform Particle
Characteristics
1.458-37-7
2.207-280-5
3.Not Available
4.Not Available
>88.14
Skin Corrosion/Irritation Category 2, Serious Eye
Damage/Eye Irritation Category 2, Reproductive Toxicity
Category 1B, Specific Target Organ Toxicity - Single
Exposure (Respiratory Tract Irritation) Category 3; H315,
H319, H360Fd, H335 [1]
Not
Available
Not Available
1.7631-86-9
2.231-545-4
3.Not Available
4.Not Available
<1.95 Not Applicable
Not
Available
Not Available
1.Not Available
2.Not Available
3.Not Available
4.Not Available
<9.79 Not Applicable
Not
Available
Not Available
Legend: 1. Classified by Chemwatch; 2. Classification drawn from GB-CLP Regulation, UK SI 2019/720 and UK SI 2020/1567; 3.
Classification drawn from C&L; * EU IOELVs available; [e] Substance identified as having endocrine disrupting properties
SECTION 4 First aid measures
4.1. Description of first aid measures
Eye Contact
If this product comes in contact with the eyes:
Wash out immediately with fresh running water.
Ensure complete irrigation of the eye by keeping eyelids apart and away from eye and moving the eyelids by occasionally
lifting the upper and lower lids.
Seek medical attention without delay; if pain persists or recurs seek medical attention.
Removal of contact lenses after an eye injury should only be undertaken by skilled personnel.
Skin Contact
If skin contact occurs:
Immediately remove all contaminated clothing, including footwear.
Flush skin and hair with running water (and soap if available).
Seek medical attention in event of irritation.
Inhalation
If fumes or combustion products are inhaled remove from contaminated area.
Lay patient down. Keep warm and rested.
Prostheses such as false teeth, which may block airway, should be removed, where possible, prior to initiating first aid
procedures.
Apply artificial respiration if not breathing, preferably with a demand valve resuscitator, bag-valve mask device, or pocket
curcumin
silica
amorphous
lipisperse
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mask as trained. Perform CPR if necessary.
Transport to hospital, or doctor, without delay.
Ingestion
If swallowed do NOT induce vomiting.
If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain open airway and
prevent aspiration.
Observe the patient carefully.
Never give liquid to a person showing signs of being sleepy or with reduced awareness; i.e. becoming unconscious.
Give water to rinse out mouth, then provide liquid slowly and as much as casualty can comfortably drink.
Seek medical advice.
4.2 Most important symptoms and effects, both acute and delayed
See Section 11
4.3. Indication of any immediate medical attention and special treatment needed
Treat symptomatically.
SECTION 5 Firefighting measures
5.1. Extinguishing media
Water spray or fog.
Foam.
Dry chemical powder.
BCF (where regulations permit).
Carbon dioxide.
5.2. Special hazards arising from the substrate or mixture
Fire Incompatibility
Avoid contamination with oxidising agents i.e. nitrates, oxidising acids, chlorine bleaches, pool chlorine etc. as ignition may
result
5.3. Advice for firefighters
Fire Fighting
When silica dust is dispersed in air, firefighters should wear inhalation protection as hazardous substances from the fire may
be adsorbed on the silica particles.
When heated to extreme temperatures, (>1700 deg.C) amorphous silica can fuse.
Alert Fire Brigade and tell them location and nature of hazard.
Wear breathing apparatus plus protective gloves.
Prevent, by any means available, spillage from entering drains or water courses.
Use water delivered as a fine spray to control fire and cool adjacent area.
DO NOT approach containers suspected to be hot.
Cool fire exposed containers with water spray from a protected location.
If safe to do so, remove containers from path of fire.
Equipment should be thoroughly decontaminated after use.
Fire/Explosion Hazard
When silica dust is dispersed in air, firefighters should wear inhalation protection as hazardous substances from the fire may
be adsorbed on the silica particles.
When heated to extreme temperatures, (>1700 deg.C) amorphous silica can fuse.
Combustible solid which burns but propagates flame with difficulty; it is estimated that most organic dusts are combustible
(circa 70%) - according to the circumstances under which the combustion process occurs, such materials may cause fires
and / or dust explosions.
Organic powders when finely divided over a range of concentrations regardless of particulate size or shape and suspended in
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air or some other oxidizing medium may form explosive dust-air mixtures and result in a fire or dust explosion (including
secondary explosions).
Avoid generating dust, particularly clouds of dust in a confined or unventilated space as dusts may form an explosive mixture
with air, and any source of ignition, i.e. flame or spark, will cause fire or explosion. Dust clouds generated by the fine grinding
of the solid are a particular hazard; accumulations of fine dust (420 micron or less) may burn rapidly and fiercely if ignited -
particles exceeding this limit will generally not form flammable dust clouds; once initiated, however, larger particles up to 1400
microns diameter will contribute to the propagation of an explosion.
In the same way as gases and vapours, dusts in the form of a cloud are only ignitable over a range of concentrations; in
principle, the concepts of lower explosive limit (LEL) and upper explosive limit (UEL) are applicable to dust clouds but only
the LEL is of practical use; - this is because of the inherent difficulty of achieving homogeneous dust clouds at high
temperatures (for dusts the LEL is often called the "Minimum Explosible Concentration", MEC).
When processed with flammable liquids/vapors/mists,ignitable (hybrid) mixtures may be formed with combustible dusts.
Ignitable mixtures will increase the rate of explosion pressure rise and the Minimum Ignition Energy (the minimum amount of
energy required to ignite dust clouds - MIE) will be lower than the pure dust in air mixture. The Lower Explosive Limit (LEL) of
the vapour/dust mixture will be lower than the individual LELs for the vapors/mists or dusts.
A dust explosion may release of large quantities of gaseous products; this in turn creates a subsequent pressure rise of
explosive force capable of damaging plant and buildings and injuring people.
Usually the initial or primary explosion takes place in a confined space such as plant or machinery, and can be of sufficient
force to damage or rupture the plant. If the shock wave from the primary explosion enters the surrounding area, it will disturb
any settled dust layers, forming a second dust cloud, and often initiate a much larger secondary explosion. All large scale
explosions have resulted from chain reactions of this type.
Dry dust can be charged electrostatically by turbulence, pneumatic transport, pouring, in exhaust ducts and during transport.
Build-up of electrostatic charge may be prevented by bonding and grounding.
Powder handling equipment such as dust collectors, dryers and mills may require additional protection measures such as
explosion venting.
All movable parts coming in contact with this material should have a speed of less than 1-meter/sec.
A sudden release of statically charged materials from storage or process equipment, particularly at elevated temperatures
and/ or pressure, may result in ignition especially in the absence of an apparent ignition source.
One important effect of the particulate nature of powders is that the surface area and surface structure (and often moisture
content) can vary widely from sample to sample, depending of how the powder was manufactured and handled; this means
that it is virtually impossible to use flammability data published in the literature for dusts (in contrast to that published for
gases and vapours).
Autoignition temperatures are often quoted for dust clouds (minimum ignition temperature (MIT)) and dust layers (layer
ignition temperature (LIT)); LIT generally falls as the thickness of the layer increases.
Combustion products include:
,
carbon monoxide (CO)
,
carbon dioxide (CO2)
,
silicon dioxide (SiO2)
,
other pyrolysis products typical of burning organic material.
May emit poisonous fumes.
May emit corrosive fumes.
SECTION 6 Accidental release measures
6.1. Personal precautions, protective equipment and emergency procedures
See section 8
6.2. Environmental precautions
See section 12
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6.3. Methods and material for containment and cleaning up
Minor Spills
Clean up waste regularly and abnormal spills immediately.
Avoid breathing dust and contact with skin and eyes.
Wear protective clothing, gloves, safety glasses and dust respirator.
Use dry clean up procedures and avoid generating dust.
Vacuum up or sweep up. NOTE: Vacuum cleaner must be fitted with an exhaust micro filter (HEPA type) (consider
explosion-proof machines designed to be grounded during storage and use).
Dampen with water to prevent dusting before sweeping.
Place in suitable containers for disposal.
Major Spills
Moderate hazard.
CAUTION: Advise personnel in area.
Alert Emergency Services and tell them location and nature of hazard.
Control personal contact by wearing protective clothing.
Prevent, by any means available, spillage from entering drains or water courses.
Recover product wherever possible.
IF DRY: Use dry clean up procedures and avoid generating dust. Collect residues and place in sealed plastic bags or other
containers for disposal. IF WET: Vacuum/shovel up and place in labelled containers for disposal.
ALWAYS: Wash area down with large amounts of water and prevent runoff into drains.
If contamination of drains or waterways occurs, advise Emergency Services.
6.4. Reference to other sections
Personal Protective Equipment advice is contained in Section 8 of the SDS.
SECTION 7 Handling and storage
7.1. Precautions for safe handling
Safe handling
Avoid all personal contact, including inhalation.
Wear protective clothing when risk of exposure occurs.
Use in a well-ventilated area.
Prevent concentration in hollows and sumps.
DO NOT enter confined spaces until atmosphere has been checked.
DO NOT allow material to contact humans, exposed food or food utensils.
Avoid contact with incompatible materials.
When handling, DO NOT eat, drink or smoke.
Keep containers securely sealed when not in use.
Avoid physical damage to containers.
Always wash hands with soap and water after handling.
Work clothes should be laundered separately. Launder contaminated clothing before re-use.
Use good occupational work practice.
Observe manufacturer's storage and handling recommendations contained within this SDS.
Atmosphere should be regularly checked against established exposure standards to ensure safe working conditions are
maintained.
Organic powders when finely divided over a range of concentrations regardless of particulate size or shape and suspended in
air or some other oxidizing medium may form explosive dust-air mixtures and result in a fire or dust explosion (including
secondary explosions)
Minimise airborne dust and eliminate all ignition sources. Keep away from heat, hot surfaces, sparks, and flame.
Establish good housekeeping practices.
Remove dust accumulations on a regular basis by vacuuming or gentle sweeping to avoid creating dust clouds.
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Use continuous suction at points of dust generation to capture and minimise the accumulation of dusts. Particular attention
should be given to overhead and hidden horizontal surfaces to minimise the probability of a "secondary" explosion. According
to NFPA Standard 654, dust layers 1/32 in.(0.8 mm) thick can be sufficient to warrant immediate cleaning of the area.
Do not use air hoses for cleaning.
Minimise dry sweeping to avoid generation of dust clouds. Vacuum dust-accumulating surfaces and remove to a chemical
disposal area. Vacuums with explosion-proof motors should be used.
Control sources of static electricity. Dusts or their packages may accumulate static charges, and static discharge can be a
source of ignition.
Solids handling systems must be designed in accordance with applicable standards (e.g. NFPA including 654 and 77) and
other national guidance.
Do not empty directly into flammable solvents or in the presence of flammable vapors.
The operator, the packaging container and all equipment must be grounded with electrical bonding and grounding systems.
Plastic bags and plastics cannot be grounded, and antistatic bags do not completely protect against development of static
charges.
Empty containers may contain residual dust which has the potential to accumulate following settling. Such dusts may explode in
the presence of an appropriate ignition source.
Do NOT cut, drill, grind or weld such containers.
In addition ensure such activity is not performed near full, partially empty or empty containers without appropriate workplace
safety authorisation or permit.
Fire and explosion
protection
See section 5
Other information
Phenylpropanoids are labile and after unsealing the container, they should be stored refrigerated or frozen under an inert gas
such as nitrogen/argon.
Phenylpropanoids are easily oxidised in the liquid state and should be used them within a short period of time after preparation.
As long as no special remark is mentioned in the catalogues or labels, they can be stored at room temperature. Solids can be
stored longer than liquid compounds or solutions.
Compounds with phenolic hydroxy groups can gradually change colour from brown to black while being stored.
Compounds with aldehyde groups are also apt to be oxidized to carboxylic acids.
Consider storage under inert gas.
Store in original containers.
Keep containers securely sealed.
Store in a cool, dry area protected from environmental extremes.
Store away from incompatible materials and foodstuff containers.
Protect containers against physical damage and check regularly for leaks.
Observe manufacturer's storage and handling recommendations contained within this SDS.
For major quantities:
Consider storage in bunded areas - ensure storage areas are isolated from sources of community water (including
stormwater, ground water, lakes and streams}.
Ensure that accidental discharge to air or water is the subject of a contingency disaster management plan; this may require
consultation with local authorities.
7.2. Conditions for safe storage, including any incompatibilities
Suitable container
Glass container is suitable for laboratory quantities
Polyethylene or polypropylene container.
Check all containers are clearly labelled and free from leaks.
Storage incompatibility
The substance may be or contains a "metalloid"
The following elements are considered to be metalloids; boron,silicon, germanium, arsenic, antimony, tellurium and (possibly)
polonium
The electronegativities and ionisation energies of the metalloids are between those of the metals and nonmetals, so the
metalloids exhibit characteristics of both classes. The reactivity of the metalloids depends on the element with which they are
reacting. For example, boron acts as a nonmetal when reacting with sodium yet as a metal when reacting with fluorine.
Unlike most metals, most metalloids are amphoteric- that is they can act as both an acid and a base. For instance, arsenic forms
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not only salts such as arsenic halides, by the reaction with certain strong acid, but it also forms arsenites by reactions with strong
bases.
Most metalloids have a multiplicity of oxidation states or valences. For instance, tellurium has the oxidation states +2, -2, +4, and
+6. Metalloids react like non-metals when they react with metals and act like metals when they react with non-metals.
Silicas:
react with hydrofluoric acid to produce silicon tetrafluoride gas
react with xenon hexafluoride to produce explosive xenon trioxide
reacts exothermically with oxygen difluoride, and explosively with chlorine trifluoride (these halogenated materials are not
commonplace industrial materials) and other fluorine-containing compounds
may react with fluorine, chlorates
are incompatible with strong oxidisers, manganese trioxide, chlorine trioxide, strong alkalis, metal oxides, concentrated
orthophosphoric acid, vinyl acetate
may react vigorously when heated with alkali carbonates.
Avoid strong acids, bases.
Avoid reaction with oxidising agents
7.3. Specific end use(s)
See section 1.2
SECTION 8 Exposure controls / personal protection
8.1. Control parameters
Ingredient
DNELs
Exposure Pattern Worker
PNECs
Compartment
silica amorphous Inhalation 0.3 mg/m³ (Local, Chronic) Not Available
* Values for General Population
Occupational Exposure Limits (OEL)
INGREDIENT DATA
Source Ingredient Material name TWA STEL Peak Notes
UK Workplace Exposure
Limits (WELs).
silica
amorphous
Silica, fused respirable dust
0.08
mg/m3
Not
Available
Not
Available
Not
Available
UK Workplace Exposure
Limits (WELs).
silica
amorphous
Diatomaceous earth, natural, respirable
dust
1.2 mg/m3
Not
Available
Not
Available
Not
Available
Emergency Limits
Ingredient TEEL-1 TEEL-2 TEEL-3
silica amorphous 18 mg/m3 200 mg/m3 1,200 mg/m3
silica amorphous 18 mg/m3 100 mg/m3 630 mg/m3
silica amorphous 120 mg/m3 1,300 mg/m3 7,900 mg/m3
Ingredient Original IDLH Revised IDLH
curcumin Not Available Not Available
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Ingredient Original IDLH Revised IDLH
silica amorphous 3,000 mg/m3 Not Available
lipisperse Not Available Not Available
Occupational Exposure Banding
Ingredient Occupational Exposure Band Rating Occupational Exposure Band Limit
curcumin E ≤ 0.01 mg/m³
Notes: Occupational exposure banding is a process of assigning chemicals into specific categories or bands based on a chemical's
potency and the adverse health outcomes associated with exposure. The output of this process is an occupational exposure
band (OEB), which corresponds to a range of exposure concentrations that are expected to protect worker health.
8.2. Exposure controls
8.2.1. Appropriate
engineering controls
Enclosed local exhaust ventilation is required at points of dust, fume or vapour generation.
HEPA terminated local exhaust ventilation should be considered at point of generation of dust, fumes or vapours.
Barrier protection or laminar flow cabinets should be considered for laboratory scale handling.
A fume hood or vented balance enclosure is recommended for weighing/ transferring quantities exceeding 500 mg.
When handling quantities up to 500 gram in either a standard laboratory with general dilution ventilation (e.g. 6-12 air changes
per hour) is preferred. Quantities up to 1 kilogram may require a designated laboratory using fume hood, biological safety
cabinet, or approved vented enclosures. Quantities exceeding 1 kilogram should be handled in a designated laboratory or
containment laboratory using appropriate barrier/ containment technology.
Manufacturing and pilot plant operations require barrier/ containment and direct coupling technologies.
Barrier/ containment technology and direct coupling (totally enclosed processes that create a barrier between the equipment and
the room) typically use double or split butterfly valves and hybrid unidirectional airflow/ local exhaust ventilation solutions (e.g.
powder containment booths). Glove bags, isolator glove box systems are optional. HEPA filtration of exhaust from dry product
handling areas is required.
Fume-hoods and other open-face containment devices are acceptable when face velocities of at least 1 m/s (200 feet/minute)
are achieved. Partitions, barriers, and other partial containment technologies are required to prevent migration of the material to
uncontrolled areas. For non-routine emergencies maximum local and general exhaust are necessary. Air contaminants
generated in the workplace possess varying "escape" velocities which, in turn, determine the "capture velocities" of fresh
circulating air required to effectively remove the contaminant.
Type of Contaminant: Air Speed:
solvent, vapours, etc. evaporating from tank (in still air)
0.25-0.5 m/s
(50-100 f/min.)
aerosols, fumes from pouring operations, intermittent container filling, low speed conveyer transfers
(released at low velocity into zone of active generation)
0.5-1 m/s (100-200
f/min.)
direct spray, drum filling, conveyer loading, crusher dusts, gas discharge (active generation into zone
of rapid air motion)
1-2.5 m/s (200-500
f/min.)
Within each range the appropriate value depends on:
Lower end of the range Upper end of the range
1: Room air currents minimal or favourable to capture 1: Disturbing room air currents
2: Contaminants of low toxicity or of nuisance value only. 2: Contaminants of high toxicity
3: Intermittent, low production. 3: High production, heavy use
4: Large hood or large air mass in motion 4: Small hood-local control only
Simple theory shows that air velocity falls rapidly with distance away from the opening of a simple extraction pipe. Velocity
generally decreases with the square of distance from the extraction point (in simple cases). Therefore the air speed at the
extraction point should be adjusted, accordingly, after reference to distance from the contaminating source. The air velocity at the
extraction fan, for example, should be a minimum of 1-2.5 m/s (200-500 f/min.) for extraction of gases discharged 2 meters
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distant from the extraction point. Other mechanical considerations, producing performance deficits within the extraction
apparatus, make it essential that theoretical air velocities are multiplied by factors of 10 or more when extraction systems are
installed or used.
The need for respiratory protection should also be assessed where incidental or accidental exposure is anticipated: Dependent
on levels of contamination, PAPR, full face air purifying devices with P2 or P3 filters or air supplied respirators should be
evaluated.
The following protective devices are recommended where exposures exceed the recommended exposure control guidelines by
factors of:
10; high efficiency particulate (HEPA) filters or cartridges
10-25; loose-fitting (Tyvek or helmet type) HEPA powered-air purifying respirator.
25-50; a full face-piece negative pressure respirator with HEPA filters
50-100; tight-fitting, full face-piece HEPA PAPR
100-1000; a hood-shroud HEPA PAPR or full face-piece supplied air respirator operated in pressure demand or other positive
pressure mode.
8.2.2. Personal protection
Eye and face protection
When handling very small quantities of the material eye protection may not be required.
For laboratory, larger scale or bulk handling or where regular exposure in an occupational setting occurs:
Chemical goggles.
Face shield. Full face shield may be required for supplementary but never for primary protection of eyes.
Contact lenses may pose a special hazard; soft contact lenses may absorb and concentrate irritants. A written policy
document, describing the wearing of lenses or restrictions on use, should be created for each workplace or task. This should
include a review of lens absorption and adsorption for the class of chemicals in use and an account of injury experience.
Medical and first-aid personnel should be trained in their removal and suitable equipment should be readily available. In the
event of chemical exposure, begin eye irrigation immediately and remove contact lens as soon as practicable. Lens should
be removed at the first signs of eye redness or irritation - lens should be removed in a clean environment only after workers
have washed hands thoroughly. [CDC NIOSH Current Intelligence Bulletin 59], [AS/NZS 1336 or national equivalent]
Skin protection See Hand protection below
Hands/feet protection
The selection of suitable gloves does not only depend on the material, but also on further marks of quality which vary from
manufacturer to manufacturer. Where the chemical is a preparation of several substances, the resistance of the glove material
can not be calculated in advance and has therefore to be checked prior to the application.
The exact break through time for substances has to be obtained from the manufacturer of the protective gloves and has to be
observed when making a final choice.
Personal hygiene is a key element of effective hand care. Gloves must only be worn on clean hands. After using gloves, hands
should be washed and dried thoroughly. Application of a non-perfumed moisturiser is recommended.
Suitability and durability of glove type is dependent on usage. Important factors in the selection of gloves include:
· frequency and duration of contact,
· chemical resistance of glove material,
· glove thickness and
· dexterity
Select gloves tested to a relevant standard (e.g. Europe EN 374, US F739, AS/NZS 2161.1 or national equivalent).
· When prolonged or frequently repeated contact may occur, a glove with a protection class of 5 or higher (breakthrough time
greater than 240 minutes according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended.
· When only brief contact is expected, a glove with a protection class of 3 or higher (breakthrough time greater than 60 minutes
according to EN 374, AS/NZS 2161.10.1 or national equivalent) is recommended.
· Some glove polymer types are less affected by movement and this should be taken into account when considering gloves for
long-term use.
· Contaminated gloves should be replaced.
As defined in ASTM F-739-96 in any application, gloves are rated as:
· Excellent when breakthrough time > 480 min
· Good when breakthrough time > 20 min
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· Fair when breakthrough time < 20 min
· Poor when glove material degrades
For general applications, gloves with a thickness typically greater than 0.35 mm, are recommended.
It should be emphasised that glove thickness is not necessarily a good predictor of glove resistance to a specific chemical, as the
permeation efficiency of the glove will be dependent on the exact composition of the glove material. Therefore, glove selection
should also be based on consideration of the task requirements and knowledge of breakthrough times.
Glove thickness may also vary depending on the glove manufacturer, the glove type and the glove model. Therefore, the
manufacturers technical data should always be taken into account to ensure selection of the most appropriate glove for the task.
Note: Depending on the activity being conducted, gloves of varying thickness may be required for specific tasks. For example:
· Thinner gloves (down to 0.1 mm or less) may be required where a high degree of manual dexterity is needed. However, these
gloves are only likely to give short duration protection and would normally be just for single use applications, then disposed of.
· Thicker gloves (up to 3 mm or more) may be required where there is a mechanical (as well as a chemical) risk i.e. where there
is abrasion or puncture potential
Gloves must only be worn on clean hands. After using gloves, hands should be washed and dried thoroughly. Application of a
non-perfumed moisturiser is recommended.
Rubber gloves (nitrile or low-protein, powder-free latex, latex/ nitrile). Employees allergic to latex gloves should use nitrile
gloves in preference.
Double gloving should be considered.
PVC gloves.
Change gloves frequently and when contaminated, punctured or torn.
Wash hands immediately after removing gloves.
Protective shoe covers. [AS/NZS 2210]
Head covering.
Experience indicates that the following polymers are suitable as glove materials for protection against undissolved, dry solids,
where abrasive particles are not present.
polychloroprene.
nitrile rubber.
butyl rubber.
fluorocaoutchouc.
polyvinyl chloride.
Gloves should be examined for wear and/ or degradation constantly.
Body protection See Other protection below
Other protection
For quantities up to 500 grams a laboratory coat may be suitable.
For quantities up to 1 kilogram a disposable laboratory coat or coverall of low permeability is recommended. Coveralls should
be buttoned at collar and cuffs.
For quantities over 1 kilogram and manufacturing operations, wear disposable coverall of low permeability and disposable
shoe covers.
For manufacturing operations, air-supplied full body suits may be required for the provision of advanced respiratory
protection.
Eye wash unit.
Ensure there is ready access to an emergency shower.
For Emergencies: Vinyl suit
Respiratory protection
Particulate. (AS/NZS 1716 & 1715, EN 143:2000 & 149:001, ANSI Z88 or national equivalent)
Required Minimum Protection Factor Half-Face Respirator Full-Face Respirator Powered Air Respirator
up to 10 x ES
P1
Air-line*
-
-
PAPR-P1
-
up to 50 x ES Air-line** P2 PAPR-P2
up to 100 x ES - P3 -
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Air-line* -
100+ x ES - Air-line** PAPR-P3
* - Negative pressure demand ** - Continuous flow
A(All classes) = Organic vapours, B AUS or B1 = Acid gasses, B2 = Acid gas or hydrogen cyanide(HCN), B3 = Acid gas or hydrogen cyanide(HCN), E = Sulfur
dioxide(SO2), G = Agricultural chemicals, K = Ammonia(NH3), Hg = Mercury, NO = Oxides of nitrogen, MB = Methyl bromide, AX = Low boiling point organic
compounds(below 65 degC)
· Respirators may be necessary when engineering and administrative controls do not adequately prevent exposures.
· The decision to use respiratory protection should be based on professional judgment that takes into account toxicity information, exposure measurement data,
and frequency and likelihood of the worker's exposure - ensure users are not subject to high thermal loads which may result in heat stress or distress due to
personal protective equipment (powered, positive flow, full face apparatus may be an option).
· Published occupational exposure limits, where they exist, will assist in determining the adequacy of the selected respiratory protection. These may be
government mandated or vendor recommended.
· Certified respirators will be useful for protecting workers from inhalation of particulates when properly selected and fit tested as part of a complete respiratory
protection program.
· Where protection from nuisance levels of dusts are desired, use type N95 (US) or type P1 (EN143) dust masks. Use respirators and components tested and
approved under appropriate government standards such as NIOSH (US) or CEN (EU)
· Use approved positive flow mask if significant quantities of dust becomes airborne.
· Try to avoid creating dust conditions.
8.2.3. Environmental exposure controls
See section 12
SECTION 9 Physical and chemical properties
9.1. Information on basic physical and chemical properties
Appearance
Air sensitive.
A diarylheptenoid (also known as diphenylheptanoid). This family consists of two aromatic rings (aryl groups) joined by a seven
carbons chain (heptane) and having various substituents. They can be classified into linear (curcuminoids) and cyclic
diarylheptanoids.
A curcuminoid is a linear diarylheptanoid, with molecules such as curcumin or derivatives of curcumin with different chemical
groups that have been formed to increase solubility of curcumins and make them suitable for drug formulation. These
compounds are natural phenols and produce a pronounced yellow colour. Curcuminoids are soluble in dimethyl sulfoxide
(DMSO), acetone and ethanol but are poorly soluble in lipids. It is possible to increase curcuminoid solubility in aqueous phase
with surfactants or co-surfactants.
Curcuminoids form a more stable complex with solutions which contain cyclodextrin towards hydrolytic degradations. The stability
differs between size and characterization of the cyclodextrins that are used.
Designated as an aromatic polyketide a compounds in which carbon chains are extended with malonyl-CoA onto
phenylpropanoids.
The polyketides are further categorised as:
· Diarylheptanoids which are biosynthesized from two cinnamyl-CoA units and one malonyl-CoA. Their two
aromatic rings are connected with an aliphatic seven-carbon chain.
· Stilbenoids, chalconoids, flavonoids and isoflavonoids which are formed from a cinnamyl-CoA with three
malonyl-CoA units. Chalconoids, flavonoids and isoflavonoids possess a C6-C3-C6 skeleton whereas stilbenoids have a
C6-C2-C6skeleton which arises by decarboxylation during the biosynthesis.
A phenylpropanoid derivative - a natural organic compound of plant origin biosynthesised via the shikimic acid pathway.
Phenylalanine and tyrosine are their precursors. Phenylpropanoids comprise a group of compounds with side-chains of three
carbons attached to a benzene ring.
Phenylpropanoids are generally soluble in many organic solvents. They can be rather difficult to dissolve in non-polar solvents
such as hexane but dissolve well in high polar solvents such as chloroform, methanol and DMSO. Compounds with carboxyl or
phenolic hydroxy groups are soluble in aqueous alkaline solutions.
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They can be further subdivided into groups described as:
· Cinnamic acid and esters
· Cinnamic acid derivatives
· Cinnamaldehydes
· Phenylpropenes
· Coumarins
Physical state Divided Solid|Powder
Relative density (Water =
1)
Not Available
Odour Not Available
Partition coefficient
n-octanol / water
Not Available
Odour threshold Not Available
Auto-ignition temperature
(°C)
Not Available
pH (as supplied) Not Available
Decomposition
temperature (°C)
Not Available
Melting point / freezing
point (°C)
Not Available Viscosity (cSt) Not Available
Initial boiling point and
boiling range (°C)
Not Available Molecular weight (g/mol) Not Available
Flash point (°C) Not Available Taste Not Available
Evaporation rate Not Available Explosive properties Not Available
Flammability Not Available Oxidising properties Not Available
Upper Explosive Limit (%) Not Available
Surface Tension (dyn/cm
or mN/m)
Not Applicable
Lower Explosive Limit (%) Not Available Volatile Component (%vol) Not Available
Vapour pressure (kPa) Not Available Gas group Not Available
Solubility in water Miscible
pH as a solution (Not
Available%)
Not Available
Vapour density (Air = 1) Not Available VOC g/L Not Available
Nanoform Solubility Not Available
Nanoform Particle
Characteristics
Not Available
Particle Size Not Available
9.2. Other information
Not Available
SECTION 10 Stability and reactivity
10.1.Reactivity See section 7.2
10.2. Chemical stability
Unstable in the presence of incompatible materials.
Product is considered stable.
Hazardous polymerisation will not occur.
10.3. Possibility of
hazardous reactions
See section 7.2
10.4. Conditions to avoid See section 7.2
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