3. ANTIBIOTICS
These are products obtained from microorganisms and
have prominent antitumor activity.
Practically all of them intercalate between DNA strands and
interfere with its template function.
4. S.No DRUGS MOA USES ADRS
1. Actinomycin D
(Dactinomycin) :
15 μg/kg i.v. daily for 5
days.
Blocking of RNA transcription by
interfering with template function of
DNA – also single strand break in DNA
Wilm’s tumour ,
Mtx resistant
choriocarcinoma
vomiting
stomatitis
diarrhea, erythema,
alopecia and bone
marrow depression.
2. Daunorubicin
(Rubidomycin),
Doxorubicin
Anti tumor antibiotics with quite similar
chemical structures -Intercalate
between DNA strands – block DNA and
RNA synthesis; also strand breakage of
DNA.
Doxorubicin: Treat
cancers like breast
cancer,bladder
cancer,lymphoma,and
acute lymphocytic
leukaemia.
Daunorubicin: Acute
leukaemia
Cardiotoxicity,
Marrow depression,
Stomatitis,
vomiting
local tissue damage
3. Bleomycin :
30 mg twice weekly i.v.
or i.m.
(total dose 300–400
mg)
A DNA-bleomycin-Fe2+ complex appears
to undergo oxidation to bleomycin-Fe3+ .
The liberated electrons react with
oxygen to form superoxide or hydroxyl
radicals, which in turn attack the
phosphodiester bonds of DNA, resulting
in strand breakage and chromosomal
aberrations
Testicular tumor,
squamous cell carcinoma
Thickening of skin,
vomiting,
loss of appetite,
swelling of fingers
5. Miscellaneous agents
This drugs have been developed by random synthesis
and testing for antitumor activity except (L-
asparaginase)
6. S.
no
DRUGS MOA USES ADRS
1. Hydroxyurea :
20–30 mg/kg daily or 80
mg/kg twice weekly
Inhibits ribonucleoside
diphosphate reductase – so
blocks conversion of
ribonucleotides to
deoxyribonucleotide (S
specific action)
chronic myeloid
leukaemia,
Psoriasis,
sickle cell anemia
Myelosuppression,
GI disturbances,
Cutaneous reaction
2. L- Asparaginase :Isolated
from E-coli
50–200 KU/kg i.v. daily
for 2–4 weeks
It inhibit the synthesis of L-
Asparagines to L-aspartic acid
which cause the cell death.
Acute lymphoblastic
Leukaemia, Combination
therapy, non-lymphocytic
cancers.
Liver damage,
pancreatitis & CNS
symptoms (due to
protein synthesis)
3. Arsenic trioxide :It has
been a traditional poison
for ages
Same as hydroxyurea- Acute Promyelocytic
Leukemia (APL)
N/V ,hyperglycemia,
QT prolongation, A-V
block.
4. Tretinoin : Vitamin A
derivate.
Known as All trans -
retinoic acid
Highly effective in
treating Acute
Promyelocytic Leukemia
Dryness of skin, eye,
nose, mouth, pruritus,
epistaxis, rise in serum
lipids
7. ANTINEOPLASTIC
AGENTS
INTRODUCTION:
In the recent years fundamental
studies of cancer biology and
molecular mechanisms of
carcinogenesis have identified several
targets which can be attacked to
selectively kill or inhibit cancer cells
.Designing and development of drugs
to attack these targets is an active
area of current research.
These drugs primarily of 2 types
:Drugs attacking cell surface targets
or tumor antigens - specific
monoclonal antibodies. (given
parenterally)Drugs affecting cancer
specific enzymes or pathways –
synthetic molecular compounds.
(given orally)
8. DRUG & MOA USE ADVERSE EFFECTS DOSE
TYROSINE KINASE INHIBITOR
Imatinib : tyr kinase of chronic myeloid
leukaemia (CML) cells
CML Vomiting ,abdominal pain 400 mg/day c̅ meals
(600-800 mg/day in
accelerated phase of
CML)
EPIDERMAL GROWTH FACTOR (EGF)receptor
inhibitors
Gefitinib: inhibits cellular growth &
proliferation
Non small cell lung
cancer
Rash ,Diarrhoea, nausea 250 mg/day orally
ANGIOGENESIS INHIBITOR
Bevacizumab(vascular endothelium growth
inhibitor):binds to VEGF &blocks its binding to
receptor
Sorafenib(VEGF Inhibitor)
Renal cell cancer
Lung cancer
Breast cancer
Hepatocellular
carcinoma
HTN,thrombo
embolism,bleeding
5-10 mg/kg iv infusion
400 mg BD or OD
PROTEASOME INHIBITOR
Bortezomib:Binds Proteasome & it inhibits
proteolytic activity that promotes cell proliferation
and apoptosis
Multiple myeloma Peripheral neuropathy 1.3 mg/m2 i.v. bolus
injection
MONOCLONAL ANTIBODIES
Rituximab:Binds to antigen on surface of B
lymphocytes & B cell lymphoma
B cell lymphoma Infusion reaction 500 mg/m2
10. s.no DRUGS MOA USES ADRS
1. GLUCOCORTICOIDS:
Predisolone:
5-60mg/day oral,
10-40mg i.m ,i.a topically
GCs interact with intracellular receptors to
inhibit the transcription of specific genes that
code for various cytokines esp. IL-2.
Autoimmune
diseases,breast
cancer,malignant
haemolysis
Osteoporosis,Cushing’s
Syndrome
2. ESTROGENS:
Fosfestrol:
600-1200 mg i.v initially
120-240 mg orally
Competitively binds to the androgen receptors-
Form drug-receptor complex & inhibits the
action of androgens & also hormone induced
growth of cancer cells
Prostate cancer N/V,cardiovascular
complications ,blood
clots edema & genital
skin reactions
3. SERM’S :
Tamoxifen :
Potent ER antagonist
Competitive inhibitor of estradiol binding to
the ER Binding of estradiol & SERM to the
estrogen binding sites of the ER’s initiate a
change in conformation of the ER, dissociates
the ER form heat-shock proteins and inhibition
of ER dimerisation
Breast cancer N/ V, Vaginal bleeding,
Thromboembolism,
Vision changes
4. Selective Estrogen
Receptor Down
regulator (SERD):
Fulvestrant: 500 mg on
day 1 (IM route)
Inhibits ER dimerization & prevents interaction
of ER with DNA
ER is down regulated resulting in more
complete supression of ER responsive gene
function
Breast cancer Nausea,Asthma,Pain,
Vasodilation,
Headache
11. S.No DRUGS MOA USES ADRS
5. AROMATASE
INHIBITORS:
Letrozole:
2.5mg OD oral
Anastrozole:
1mg OD
an orally active nonsteroidal
compound Inhibits aromatization all
over the body, including that within
the breast cancer cells, resulting in
nearly total estrogen deprivation
Advanced
breast cancer,
early breast
cancer
Dyspesia,hot flushes,
bone loss, diarrhea
Vaginal dryness,
bleeding
6. ANTI ANDROGENS:
Flutamide: 250 mg
competitively blocks androgen action
by inhibiting androgen uptake or
binding to it’s target tissues.
Hot flushes,
Libido,Impotency
Gynaecomastia,
Breast tenderness,
7. 5-α REDUCTASE
INHIBITORS :
Finasteride:1mg
A competitive inhibitor of the enzyme
5α - reductase which converts
testosterone into more active
DHT(Dihydrotestosterone) responsible
for androgen action in many tissues
including the prostate gland & hair
follicles.
Decreases libido,skin
rashes,impolency,
gynaecomastia
Dutasteride: 0.5 mg Inhibit both type 1& 2 5-α reductase
enzyme
12. S.NO DRUGS MOA USES ADRS
8. GnRH ANALOUGES:
Nafarelin:
↓FSH & LH release from
pituitary- ↓ the release of
estrogen & testosterone
Breast Cancer,
Prostatic Cancer
hot flushes, loss of
libido, vaginal dryness,
osteoporosis ,
emotional lability
9. PROGESTINS:
Hydroxyprogesterone:
Mifepristone:
It is a progestational
and glucocorticoid
hormone antagonist.
Its inhibition of progesterone
induces bleeding during the
luteal phase and in early
pregnancy by releasing
endogenous prostaglandins
from the endometrium
metastatic
endometrial
cancer
bleeding
Vaginal bleeding (lasts
from 8 to 17 days ) ,
abdominal pain and
uterine cramps,
nausea, vomiting, and
diarrhea
