CHEMOTHERAPY/ ANTICANCER DRUGS/ NEOPLASTIC AGENTS
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1 CHEMOTHERAPY/ 1 Oncology, Misc, Vaccines ANTICANCER DRUGS/ NEOPLASTIC AGENTS Important Terms: Cancer: A group of diseases involving abnormal cell growth with the potential to invade or spread to other parts of the body. Neoplasia: Uncontrolled growth of new tissue, the product of which is known as a tumour, and these tumours may be either malignant or benign. Malignant tumours: have the capability of invading surrounding tissues and moving to distant locations in the body in a process known as metastasis; characteristics that benign tumours do not possess. Chemotherapy: Drugs that are used to kill cells and includes both antibiotics and agents used in the treatment of cancer. Autocrine signalling: Cells may acquire the ability to synthesize their own growth factors Apoptosis: programmed cell death Apoptosome: apoptotic protease activating factor-1 (apaf-1) molecules to form a wheel-like structure of seven spokes. Drugs are used with the aim of: Cure or prolonged remission, Palliation, Adjuvant chemotherapy Treatment: o Surgery o Chemotherapy o Radiation Therapy o Hormonal Therapy o Targeted Therapy o Palliative Care Classification: [Pneumonic: AAP MATT] A. Cytotoxic Drugs 1. Alkylating agents[pmemonic: NAMENT] Nitrogen mustards: Mechlorethamine (Mustine HCl), Cyclophosphamide, Ifosfamide, Chlorambucil, Melphalan
2 3 Oncology, Misc, Vaccines C. Hormonal Drugs 1. Glucocorticoids: Prednisolone and Others 2. Estrogens: Fosfestrol, Ethinylestradiol 3. Selective Estrogen Receptor Modulators: Tamoxifen, Toremifene 4. Selective Estrogen Receptor Down Regulators: Fulvestrant 5. Aromatase Inhibitors: Letrozole, Anastrozole, Exemestane 6. Antiandrogen: Flutamide, Bicalutamide 7. 5:Α Reductase Inhibitor: Finasteride, Dutasteride 8. GnRH Analogues: Nafarelin, Leuprorelin, Triptorelin 9. Progestins: Hydroxyprogesterone Acetate etc. Based On Step of Cell Cycle Action I.Cell Cycle Nonspecific Kill Resting As Well As Dividing Cells Eg. Nitrogen Mustard, Cyclophosphamide, Chlorambucil, Carmustine, Dacarbazine, Busulfan, L- Asparaginase, Cisplatin, Procarbazine, Actinomvcin D II.Cell Cycle Specific- Kill Only Actively Dividing Cells o Their toxicity is generally expressed in s phase. o These drugs may show considerable phase selectivity, G 1 : Vinblastine S: Mtx, Cytarabine, 6-TG, 6-MP, 5-FU, Hydroxyurea, Mitomycin C, Doxorubicin, Daunorubicin G 2 : Daunorubicin, Bleomycin, Etoposide, Topotecan. [Pneumonic: DTEB] M: Vincristine, Vinblastine, Paclitaxel, Docetaxel [Pneumonic: VT]
3 4 Oncology, Misc, Vaccines Toxicity of Cytotoxic Drugs: Bone marrow Depression of bone marrow results in granulocytopenia, agranulocytosis, thrombocytopenia, aplastic anaemia GIT: Drugs cause mucositis are-bleomycin, Actinomycin D, Daunorubicin, Doxorubicin, Fluorouracil and Methotrexate. Drugs causing emesis: Cisplatin, Mustine, Cyclophosphamide, Actinomycin D, Dacarbazine, Lomustine Skin: Alopecia Gonads: Inhibition of gonadal cells causes oligozoospermia and impotence in males; inhibition of ovulation and amenorrhoea are common in females. Foetus: Teratogenesis Carcinogenicity Hyperuricaemia: Gout, urate stones, Allopurinol is protective by decreasing uric acid synthesis. Individual drug toxicity: o Neuropathy by Vincristine o Cardiomyopathy by Doxorubicin o Cystitis and Alopecia by Cyclophosphamide Individual Drugs Alkylating Agents: Produce highly reactive carbonium ion intermediates which transfer alkyl group to cellular macro-molecules by forming covalent bonds. Position 7 of guanine residues in DNA is more susceptible. Alkylation cause cross linking/abnormal base pairing/ scission of DNA strand
4 5 Oncology, Misc, Vaccines Nitrogen mustards- Nitrogen mustards are compounds similar to sulfur mustard or mustard gas developed and used in World War I. Mechlorethamine (Mustine HCl) Nitrogen mustard; highly reactive and local vesicant Only by i.v. route. Antidote: Sodium thiosulfate Cyclophosphamide Inactive, transformation into active metabolites (aldophosphamide, phosphoramide mustard) occurs in the liver Prominent immunosuppressant property Alopecia and cystitis (due to acrolein) are prominent. Chloramphenicol retards the metabolism of cyclophosphamide. Metabolic and activation of Cyclophosphamide Ifosfamide: Dose limiting toxicity is haemorrhagic cystitis. Rescue agent MESNA given. R-isomer is converted to the required 4-hydroxy-ifosfamide 2 to 3 times faster than the S-isomer MESNA [Sodium methanethiolate, Sodium 2-sulfanylethane sulfonate, 2-Mercaptoethane Sulfonate Sodium]
5 7 Oncology, Misc, Vaccines Ethylenimine- Thio-TEPA: TEPA Metabolic and chemical interactions of thiotepa with DNA Alkylsulfonate: Busulfan Hyperuricaemia, sterility. Drug of choice for chronic myeloid leukaemia Nitrosoureas: Carmustine (BCNU) Highly lipid soluble alkylating agents with a wide range of antitumor activity Cross blood-brain barrier Lomustine (CCNU) Dacarbazine (DTIC): Inhibitory action on RNA and protein synthesis (others mainly affect DNA)
6 Resistance: mismatch pair, decreased uptake Toxicity: Renal impairment, tinnitus, deafness, neuropathy, hyperuricaemia 9 Oncology, Misc, Vaccines Carboplatin Less reactive, better tolerated due to cyclic ring(1,1cyclobutane dicarboxylate) Rescue Agent: chelat 1, 1-cyclobutane-dicarboxylate Toxicity: Nephrotoxicity, ototoxicity and neurotoxicity are low. Dose-limiting toxicity is thrombocytopenia and leucopenia. Satraplatin: orally active Mechanism of cisplatin activation and formation of DNA adducts Antimetabolites: Analogues related to normal components of DNA or of coenzymes involved in nucleic acid synthesis. Competitively inhibit utilization of the normal substrate or get themselves incorporated forming dysfunctional macromolecules Folate antagonist: Methotrexate (Mtx) Oldest and highly efficacious anti-neoplastic drugs
7 10 Oncology, Misc, Vaccines Inhibits dihydrofolate reductase (DHFRase) block the conversion of dihydrofolic acid (DHFA) to tetra hydrofolic acid (THFA), an essential coenzyme required for one carbon transfer reactions in de-novo purine synthesis and amino acid inter-conversions. Inhibition is pseudo-irreversible because Mtx has 50,000 times higher affinity for the enzyme than the normal substrate. Methotrexate has cell cycle specific action kills cells in S phase; primarily inhibits DNA synthesis. Toxicity: Megaloblastic anaemia, pancytopenia Methotrexate excreted unchanged in urine. Salicylates, sulfonamides, dicumerol displace it from protein binding sites. Aspirin and sulfonamides enhance toxicity of Mtx by decreasing its renal tubular secretion. Amelioration: By folic acid, because it will not be converted to the active coenzyme form. Folinic acid (N5 formyl THFA, cirtrovorum factor) rapidly reverses the effects. Use of folinic acid rescue has permitted much higher doses of Mtx (100 times higher dose) Calcium leucovorin followed within 3 hours, repeated as required. Thymidine also counteracts Mtx toxicity. Highly effective in maintaining remission in children with acute leukemia s, malignancies, rheumatoid, athritis, psoriasis and as immunosuppressant.. Purine antagonist: 6-Mercaptopurine (6-MP) Converted in the body to mono ribonucleotides which inhibit the conversion of inosine monophosphate to adenine and guanine nucleotides
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