Antineoplastic Drugs

DR. F. O. WANGO

CANCER
 cell proliferation and differentiation.
 oncogenes and Tumuor Suppressor Genes(p53).

CELL-CYCLE KINETICS.
 targeted specific phases.

PHASES OF CELL CYCLE.
 . G0 : Resting
 G1: Precedes  S: DNA synthesis  G2: premitotic interval.  MITOTIC PHASE.

CELL CYCLE-SPECIFIC AGENTS.
 ANTIMETABOLITES.
 BLEOMYCIN PEPTIDE ANTIBIOTICS.  PODOPHYLIN ALKALOIDS  PLANT ALKALOIDS.

CELL CYCLE-NONSPECIFIC AGENTS.
 ALKYLATING AGENTS.
 ANTIBIOTICS  CISPLATIN  NITROSOUREAS

CLASSES OF ANTINEOPLASTIC AGENTS
 AKYLATING AGENTS.
 ANTIMETABOLITES  NATURAL PRODUCTS (1) Vinca Alkaloids (2) Taxanes

(3) Epipodophylotoxins (4) Antibiotics  ENZYMES  SUBSTITUTED UREA  PROTEIN KINASE INHIBITORS  HORMONE AND ANTAGONISTS

ALKYLATING AGENTS
 . Alkylating DNA cell death.
 react sulphydryl , amino , hydroxyl, carboxyl and

phosphate groups.

mechanism
 Through ethyleneimonium ion directly /carbonium

transfer an alkyl to cellular . @N7 Cross-linking of DNA.


ADVERSE EFFECTS.
 Vesicant expt activated directCyclophosphamide
 Nausea and vomitting.  Bone marrow, GIT and Gonads.

ALKYLATING AGENTS.
 Cyclophosphamide, Mechlorethemine, melphalan,

Chlorumbicil, thiotepa Busulphan. .

NITROSOUREAS
 Carmustine, lomustine and semustine are

nitrosoureas  highly lipid-soluble  cross blood-brain barrier.

DRUG RESISTANCE
 repair DNA
 Decreased alkyl permeability.  Increased glutathione inactivates the alkylating

agent.

DRUGS ACTING AS ALKYLATING
 PROCARBAZINE: Inhibits synthesis of NA a
 Hodgkins disease.  leukomonogenic, teratogenic and mutogenic.

 Dacarbazine: melanoma, hodgkin’s disease and soft

tissue sarcoma.  Cisplatin and Carboplatin: genitourinary cancers & little effect bone marrow. .