This document outlines a seminar presentation on current and novel approaches for treating dyslipidemia. It discusses the relationship between different lipids like LDL, HDL, and triglycerides and cardiovascular disease risk. It then summarizes the current drug therapies for dyslipidemia which lower LDL cholesterol through statins, bile acid sequestrants, ezetimibe, and nicotinic acid. Novel drug targets and approaches being researched are also highlighted, including monoclonal antibodies against PCSK9 to further lower LDL, as well as strategies to increase HDL through CETP inhibitors, vaccines, and HDL mimetics. The conclusion emphasizes the need for new biomarkers and trials to monitor progression of atherosclerosis with these novel therapies.
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
Dyslipidemia-latest guidlines-Review of Guidlines by Dr.Jayasoorya p gjpgkmr
Dyslipidemia newer guidelines
2019 ESC/EAS GUIDLINES FOR MANAGEMENT OF DYSLIPIDEMIA
2019 JUNE UPDATED AMERICAN COLLEGE OF CARDIOLOGY GUIDLINES FOR MANAGEMENT OF DYSLIPIDEMIA
Hypolipidaemics pharmacology with a note on Statins /Fibrates/ Sterol absorption Inhibitors/ CETP Inhibitors / Lipoprotein Lipase activators and Bile acid sequestrants
Dyslipidemia-latest guidlines-Review of Guidlines by Dr.Jayasoorya p gjpgkmr
Dyslipidemia newer guidelines
2019 ESC/EAS GUIDLINES FOR MANAGEMENT OF DYSLIPIDEMIA
2019 JUNE UPDATED AMERICAN COLLEGE OF CARDIOLOGY GUIDLINES FOR MANAGEMENT OF DYSLIPIDEMIA
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
Hyperlipidemia , dyslipidemia , and drug therapy
also Fat transport and metabolisim and pathophysiology of lipoprotein
clincal importance of
1. Hypertriglycredemia
2. Hypercholesterolemia
3.Combined hyperlipidemia
4. Some other lipoprotein disorders
Including disorder of HDL_C
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
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2 Case Reports of Gastric Ultrasound
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
CDSCO and Phamacovigilance {Regulatory body in India}NEHA GUPTA
The Central Drugs Standard Control Organization (CDSCO) is India's national regulatory body for pharmaceuticals and medical devices. Operating under the Directorate General of Health Services, Ministry of Health & Family Welfare, Government of India, the CDSCO is responsible for approving new drugs, conducting clinical trials, setting standards for drugs, controlling the quality of imported drugs, and coordinating the activities of State Drug Control Organizations by providing expert advice.
Pharmacovigilance, on the other hand, is the science and activities related to the detection, assessment, understanding, and prevention of adverse effects or any other drug-related problems. The primary aim of pharmacovigilance is to ensure the safety and efficacy of medicines, thereby protecting public health.
In India, pharmacovigilance activities are monitored by the Pharmacovigilance Programme of India (PvPI), which works closely with CDSCO to collect, analyze, and act upon data regarding adverse drug reactions (ADRs). Together, they play a critical role in ensuring that the benefits of drugs outweigh their risks, maintaining high standards of patient safety, and promoting the rational use of medicines.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
Adv. biopharm. APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMSAkankshaAshtankar
MIP 201T & MPH 202T
ADVANCED BIOPHARMACEUTICS & PHARMACOKINETICS : UNIT 5
APPLICATION OF PHARMACOKINETICS : TARGETED DRUG DELIVERY SYSTEMS By - AKANKSHA ASHTANKAR
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Are There Any Natural Remedies To Treat Syphilis.pdf
Antihyperlipidimic drug therapy-current and noval approaches.pptx
1. A
SEMINAR
ON
ANTILIPIDEMIC DRUG THERAPY-PRESENT & NOVAL APPROACHES
Presented by
Mr. MOHAMMED OBAID MOHIUDDIN
Reg, No. 170822887007
MASTERS OF PHARMACY I Yr. I Sem.
(PHARMACOLOGY)
Under the supervision of
Dr. SYED SAFIULLAH GHORI, M. Pharm, Ph.D.
DEPARTMENT OF PHARMACOLOGY
ANWARUL ULOOM COLLEGE OF PHARMACY
(A Muslim Minority Institution)
Affiliated to OU, Approved by AICTE and PCI.
New Mallepally, Hyderabad-500001, T.S
March-2023
2. CONTENTS
1. INTRODUCTION
2. DYSLIPIDAEMIA AND CARDIOVASCULAR DISEASE
a) LOW-DENSITY LIPOPROTEINS(LDL) AND CVD RISK
b) HIGH-DENSITY LIPOPROTEINS(HDL) AND CVD RISK
c) PLASMA TRIGLYCERIDES AND CVD RISK
3. CURRENT TREATMENT OF DYSLIPIDAEMIA
a) HMG-CO-REDUCTASE INHIBITORS(STATINS)
b) BILE ACID SEQUESTRANTS
c) EZETIMIBE
d) NICOTINIC ACID
4. NOVEL APPROACHES FOR THE TREATMENT OF DYSLIPIDEMIA
a) LDL AND APOLIPOPROTEIN B-LOWERING APPROACHES
b) NOVEL APPROACHES TO INCREASE HDL
5. CONCLUSION
REFRENCES
3. What is Hyperlipidemia?
• Hyperlipidemia a broad term, also called
hyperlipo-proteinemia, is a common
disorder in developed countries and is
the major cause of coronary heart
disease(CHD).
• It results from abnormalities in lipid
metabolism or plasma lipid transport or
a disorder in the synthesis and
degradation of plasma lipoproteins.
1. INTRODUCTION
4. Causes of hyperlipidemia
• Mostly hyperlipidemia is caused by
lifestyle habits or treatable medical
conditions.
• Obesity, not exercising, and smoking,
diabetes, obstructive jaundice, and an
under active thyroid gland inherit
hyperlipidemia.
5. What are Lipids?
Lipids are the heterogenous mixtures of
fatty acids and alcohol that are present in
the body. The major lipids in the
bloodstream are cholesterol and it's
esters, triglycerides and phospholipids.
6. Cholesterol:
A waxy, fat-like substance made in the
liver, and found in the blood and in all cells
of the body. Cholesterol is important for
good health and is needed for making cell
walls, tissues, hormones, vitamin D, and
bile acid.
7. triglycerides:
Triglycerides are a type of fat. They are
the most common type of fat in your
body. They come from foods, especially
butter, oils, and other fats you eat.
Triglycerides also come from extra
calories. These are the calories that you
eat, but your body does not need right
away.
8. What are lipoproteins?
• A lipoprotein contains both proteins
and lipids, bound to another proteins
which is called apolipoproteins, which
allow fats to move through the water
inside and outside cells.
**provide structural support and stability,
binds to receptors.
10. 2. DYSLIPIDAEMIA & CARDIOVASCULAR DISEASES
2.1 Low-Density Lipoproteins and CVD Risk:
• Dyslipidaemia is defined as a spectrum of deviations from lipid homeostasis characterized by
elevations in plasma concentrations of low-density lipoproteins (LDL), lipoprotein a ,
apolipoproteins B and triglycerides , as well as decreased plasma levels of high-density
lipoproteins (HDL) or apolipoprotein A1.
• Epidemiological studies have shown continuous relationship between total plasma
cholesterol levels and the risk of coronary heart disease1% reduction in plasma LDL-C/non-
HDL-C correlates to a 1% reduction in CVD events, whereas the increase of HDL-C by 1%
decreases CVD events by 3%.
11. 2.2 High-Density Lipoproteins and CVD Risk:
• The relationship between total plasma cholesterol and CHD risk is continuous but not
linear; the risk for CHD rises more strongly at higher LDL-C levels.
• HDL is a mediator of cholesterol transport from peripheral tissues to the liver and is
considered as an important regulator of CHD risk with an inverse relationship of HDL levels
to CHD risk.
12.
13. 2.3 Plasma Triglycerides and CVD:
• Regarding a causative role of TG for CVD events, the picture is as well not really clear.
Observational epidemiological studies and clinical trials using drugs targeting elevated
TG levels and low HDL-C levels indicate a causative and predictive role of elevated TG
plasma levels for the development of primary CHD.
• TG levels could still be a risk factor in people but of lower importance for the total risk
of coronary events.
14. 3. Current Treatment of Dyslipidaemia
Today the armamentarium introduced in medical practice for the treatment of lipid disorders
comprises five different modes of action and respective molecular targets with overall 24
different drug entities on the market, some of them available only in selected countries.
The majority of approaches focus on the reduction of LDL-C levels by inhibition of cholesterol
biosynthesis (HMG-CoA reductase inhibitors – statins), interruption of the enterohepatic
circulation of bile acids (bile acid sequestrants), or inhibition of intestinal cholesterol
absorption (ezetimibe).
Nicotinic acid and derivatives thereof as well as agonists of the peroxisome proliferator
activator receptor PPAR-α (fibrates) are efficacious drugs to increase HDL-C levels and to
decrease elevated TG levels.
15. Lipid-modifying drugs in the market:
Class
Mode of action Efficacy parameters
LDL-C(%) HDL-C(%) TG(%)
Statins Inhibition of HMG-
CoA reductase
- (18-55) +(5-15) -(7-30)
Ezetimibe Inhibition of
cholesterol
absorption
-(18-20) +(1-4) -8
Sequestrants Inhibition of bile acid
reabsorption
-(9-28) +(0-9) +(2-16)
Nicotinic Acid Multiple targets -(5-25) +(15-35) -(20-50)
16. 3.1 HMG-Co-Reductase Inhibitors (Statins):
• The molecular target of statins is the enzyme 3-hydroxy-3-
methylglutaryl-coenzyme A reductase(HMG CoA reductase) , the
rate-limiting enzyme in the biosynthesis pathway from mevalonate
to cholesterol, sterols, isoprenoids, and other lipids like dolichol and
ubiquinone.
• Statins are competitive enzyme inhibitors competing with HMG CoA
reductase for the catalytic binding site, thereby reducing
biosynthesis rate of mevalonate and its downstream products like
cholesterol.
• The decrease in the intracellular cholesterol regulatory pool leads to
an upregulation of LDL receptors in the hepatocyte plasma
membrane, leading to an increased clearance rate of LDL particles
from the blood and therefore a fall of plasma LDL-C levels.
17. Limitations :
• Statins inhibit inflammatory processes with reduction of circulating CRP levels.
• Since inhibition of the biosynthesis cascade to cholesterol by statins occurs at a very early
step, a potential risk was seen due to the decrease of other lipids like ubiquinone and
dolichol and manifestation of these decreases of non-sterol lipids in adverse side effects in
different organs including the liver, muscle, eye, or brain.
• A poor compliance due to discomfort and side effects; still around 50% of statin treated
patients discontinue their therapy after only 1 year.
• Inefficiency of a drug class or statin intolerance.
18. 3.2 Bile Acid Sequestrants (bile acid reabsorption):
• Bile acid sequestrants are polymeric anion-binding resins that
strongly bind the negatively charged bile acids in the lumen of the
small intestine, thereby interrupting the enterohepatic circulation of
bile acids.
• By blocking intestinal bile acid reabsorption, the amount and/or
composition of bile acids recirculating to the liver is changed, leading
to an increase in hepatic bile acid synthesis from cholesterol.
• the depletion of the regulatory hepatic cholesterol pool induces a
stimulation of cholesterol biosynthesis via upregulation of HMG-CoA
reductase and LDL-receptor expression at the hepatocyte surface,
the latter leading to an increase in hepatocellular uptake of LDL
particles with a consequent decrease of plasma LDL-cholesterol
levels.
19. Limitations:
1. Increased secretion of incretins like glucagon-like peptide-1(GLP-1) due to spill over of bile
acids into the colon.
2. Changes in the composition of the bile acid pool with activation of FXR receptor (regulates
bile acid synthesis, conjugation, and transport, as well as various aspects of lipid and glucose
metabolism) which results in activities like repression of hepatic gluconeogenesis and
increasing of insulin sensitivity.
3. Activation of TGR5 receptor(maintains energy and bile acid homeostasis) in the colon by bile
acid spill over with stimulation of energy expenditure.
20. 3.3 Ezetimibe (Cholesterol absorption inhibitors):
• Ezetimibe exerts its hypolipidemic action by inhibiting
intestinal cholesterol absorption.
• This cause a decrease in the cholesterol delivery to the liver
which in turn clears more cholesterol from the blood.
• selective in its action (not interfere with TGs, lipid- soluble
vitamins absorption)
• The levels of LDL-C in the serum are reduced as in bile acid
sequestrants.
21. Limitations:
Ezetimibe does not show any significant adverse side effects and has no
influence on the activities of cytochrome P-450 enzymes(superfamily of enzymes), therefore
being devoid of significant pharmacokinetic interactions with other drugs.
22. 3.4 Nicotinic Acid (Multiple targets):
• The lipid profile-modifying effects of vitamin B3 – nicotinic acid or
niacin – are since nearly 60 years.
• At pharmacological doses up to 2 g/day, niacin exerts significant
changes in most of the different lipoproteins: increases in HDL-C
of 25–30% , decreases of LDL-C by 15–20%, TG by 20–40% , LP(a)
by about 30%.
• Niacin is currently the most potent drug on the market to increase
HDL-C and the only approved drug with significant reduction of
the independent CV risk factor LP(a).
• The profile of niacin with reduction of lipoproteins and reduction
of prothrombotic factors principally is close to an ideal drug target
profile to treat dyslipidemias, particularly in patients with diabetic
dyslipidemia.
23. Limitations:
• Increases in plasma levels of uric acid promoting the risk for gout attacks.
• Glucose control is negatively affected with increases of fasting blood glucose (4–17%), HbA1c
levels, insulin levels, and a decrease in insulin sensitivity for several weeks at high niacin
doses necessary to achieve the above beneficial effects on lipid patterns; normalization of
glucose controls was observed after 48 weeks indicating that short- and long-term treatment
with niacin worsens glycaemic control limiting its use particularly in patients with diabetic
dyslipidaemia.
• low doses of nicotinic acid have only minimal effects on glucose tolerance but as well only a
moderate effect on lipid profiles.
24. 4. Novel Approaches for the Treatment of Dyslipidaemias
a. Lipid-modifying drugs in clinical development: LDL-lowering (primary target):
Target Approach Drug candidate Company Development stage
PCSK9
MoAb Alirocumab Sanofi/Regeneron Phase III, under
approval
Evolocumab Amgen Phase III, under
approval
Bococizumab Pfizer/Rinat Phase III
RG7652 Roche/Genentech Phase II
LY-3015014 Eli Lilly Phase II
Adnectin BMS-962476 BMS Phase I
siRNA ALN-PCS Alnylam Phase I
Small molecule CAT-2003 Catabasis
Pharmaceuticals
Phase II
K-312 (PCSK9/
CETP-Inh)
Kowa Phase I
MTP Small
molecule
Lomitapide Aegerion Approved
SLx-4090/KD- 206 Surface Logix/ Kadmon Phase II
25. AMPK/ATP-
citrate lyase
Small
molecule
ETC-1002 Esperion Therapeutics Phase II
TR-B1 receptor Small
molecule
MGL-3196/VIA-
3196
Madrigal
Pharmaceuticals
Phase I
ApoB Antisense Mipomersen Sanofi Approved
Apo(a) Antisense ISIS-APOARx ISIS Pharmaceuticals Phase II
26. b.Lipid-modifying drugs in clinical development: HDL-increasing (primary target):
Target Approach Drug candidate Company Development stage
CETP Small molecule Anacetrapib Merck Phase III
Evacetrapib Eli Lilly Phase III
DRL-17822 Dr Reddy Phase II
DEZ-001/TA- 8995 Dezima/Mitsubishi
Tanabe
Phase II
Vaccine ATH-03 AFFIRIS Phase I
CETP/ PCSK9 Small molecule K-312 Kowa Phase I
BET Small molecule RVX-208 Resverlogix Phase II
Niacin analogue Small molecule ARI-3037MO Arisaph
Pharmaceuticals
Phase II
27. HDL mimetics Peptide-lipid complexes
MDCO-216 The Medicines
Company
Phase II
CSL 112 CSL Ltd. Phase II
CER 001 Cerenis Therapeutics Phase II
ApoE mimetic Peptide AEM-28 Capstone Therapeutics Phase I
rec-LCAT Protein replacement MEDI6012 (ACP-501) MedImmune/
AlphaCore
Phase I
FGF-21 Protein LY2405319 Eli Lilly Phase I
analogues Protein-PEG conjugate Unknown BMS Phase II
28. 5. CONCLUSION
• The introduction of statins into clinical practice with lovastatin as the first drug of this class in 1987 has
revolutionized the treatment of lipid disorders and made reduction of LDL-C as the primary goal in the treatment
of dyslipidaemia and prevention of CVD.
• The tremendous clinical efficacy of antibodies against PCSK9 to reduce LDL-C far beyond what was possible with
statins marks a potential quantum leap in the treatment of elevated LDL cholesterol levels by modification of the
PCSK9(Proprotein convertase subtilisin/kexin type 9) pathway.
• Despite the clinically established inverse relationship between HDL and CVD risk, the enormous efforts have not
yet translated these findings into effective HDL-modifying drug approaches with unequivocal clinical benefit on
CVD morbidity and mortality.
• Recent findings highlighting the functionality of HDL as probably the most relevant factors underlying the
protective effects of HDL will help to develop HDL-modifying drugs with beneficial clinical efficacy on
cardiovascular endpoints to prevent and combat atherosclerosis and its clinical consequences.
• A major need for the clinical development of novel lipid-modifying drugs is the development of new non-
invasive measurements and biomarkers for monitoring their efficacy in halting the progression or inducing
regression of atherosclerosis to allow smaller, focused clinical trials with stratified patient populations for clinical
proof-of-concept of novel drug approaches.
29. 1. Kramer W. Antilipidemic Drug Therapy Today and in the Future. Handb Exp Pharmacol. 2016;233:373-435. doi: 10.1007/164_2015_15. PMID:
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REFERENCES