Cancer Drugs PDF

Type Class Type Drugs MOA Structure DNA Alkylating Nitrogen Mustards Melphalan, Alkylates DNA. The molecule becomes Cl C2H4 N (R) Damagin Agent...

Type Class Type Drugs MOA Structure DNA Alkylating Nitrogen Mustards Melphalan, Alkylates DNA. The molecule becomes Cl C2H4 N (R) Damagin Agent Cyclophosphamide, cyclic and attaches itself to the N7 of C2H4 Cl g agent Ifosfamide, guanine. Can crosslink DNA to damage DNA Chlorambucil, Estramustine Nitrosoureas Carmustine, Alkylates the O6 of guanine. This can cause R Lomustine, Nimustine, crosslinks and DNA damage. I O Streptozocin O=N-N_II_NH-R Platinum Drugs Carboplatin, Cisplatin, Crosslinks DNA by attaching to the N7 of \ / Oxaliplatin guanine Pt / \ Miscellaneous Busulfan Remove mesylate to form R-CH2. Alkylates CH3SO3 N7 of guanine and causes DNA to cross link Detaches to form R-CH2 Procarbazine Forms ion and cation and alkylates at the Ion O6. May inhibit protein, RNA, and DNA CH3-N synthesis ||| N Cation CH3 Class Type Drug MOA Uses Antimetabolites Pyrimidine or 5-fluorouracil, Prevents the biosynthesis of normal cellular metabolites by purine capecitabine, inhibiting the conversion of cytidylic acid to 2-deoxycytidylic antimetabolites gemcitabine, acid. Effective during S-phase. DNA dependent cytarabine, azacitidine Antimitotics Taxanes Paclitaxel, Docetaxel Binds to free tubulin to produce stable Both are used microtubules. Then it inhibits microtubule for breast lung, disassembly. Microtubules arrange in ovarian.  parallel fashion. Interferes with the miotic Docetaxel is spindle needed for cell division also for stomach, prostate, head, neck Vinca Alkaloids Vinblastine, Binds to tubulin to prevent microtube Hodgkin's vincristine, vindesine, polymerization. This means that the miotic lymphoma, vinorelbine spindle cannot be formed. Opposite of lung, bladder, taxanes melanoma Antitumor Antibiotics Anthracyclines Daunorubicin, Inserts itself between base pairs vertically doxorubicin, (between the ones connected by the ribose) epirubicin, idarubicin, and cleaves the DNA mitoxantrone DNA repair enzyme PARP inhibitors Olaparib, rucaparib, Blocks DNA repair in cancer cells to cause inhibitors niraparib, iniparib, cancer cell death talazoparib Targeted Therapy Agents Class Drugs MOA Uses Dose Tyrosine Kinase Imatinib Inhibits BCR and ABL which are needed for Chronic Myelogenous CML: 400mg OD Inhibitors cancer cell proliferation, movement, and lueukemia, acute lymphocytic ALL: 600mg OD to avoid apoptosis leukemia Gefitinib Inhibits epidermal growth factor receptor Non-small cell lung cancer with (EPFR). EPFR is used by cancer cells to EGFR exon 19 deletion or exon promote DNA Synthesis, proliferation, 21 L858R mutation migration, and survival Monoclonal Trastuzumab Binds to the subdomain IV of HER2 to Breast Cancer and other IV infusion for Antibodies inhibit it. In cancer cells when HER2 is cancers where HER2 is 90min then overexpressed it leads to abnormal cell overexpressed 30min growth, survival and proliferation Pertuzumab Binds to the subdomain II of HER2 to Breast cancers where HER2 is inhibit it. It prevents HER2 from dimerizing overexpressed  with other HER receptors. Dimerization would activate other HER receptors leading to more cancer. T-DM1 emtanine is a cytotoxic agent that is HER2 breast cancer and early IV every 3 weeks cleaved from T-DM1 in HER2 (cancer cells) stage H2 breast cancer after to kill them through triggering apoptosis surgery Apoptosis Inducing Bortezomib Binds to the 26S proteasome. This Multiple myeloma, mantle cell Agents proteosome is used for breaking down lymphoma damaged proteins. When inhibited these proteins builds up and triggers stress responses which will eventually kill the cell. Angiogenesis Bevacizuma Inhibits vascular endothelial growth factor Colon, lung IV: 5-15mg/kg q2- inhibitors b (VEGF) that is used for angiogenesis. By 3W inhibiting angiogenesis tumors can not get a blood supply therefore they starve to death. Multiple targeted Sunitinib Inhibits VEGFR (starves tumor), platelet Renal cell carcinoma, imatinib tyrosine kinase derived growth factor (inhibits stable blood resistant GI stromal tumor, inhibitor vessel growth), colony stimulating factor, pancreatic cancer and tyrosine protein kinase (prevents growth and survival) Immunotherapies Class Drug MOA PD-1 Inhibitors Pembrolizumab Inhibits PD-1 which is a surface protein on T-cells. When PD-1 and PD-L1 bind Nivolumab the tumor cell cannot be killed. So by inhibiting PD-1 the tumor can be killed Cemiplimab PD-L1 Inhibitors Atezolizumab Inhibits PD-L1 which is a transmembrane protein on cells. When PD-1 and PD-L1 Avelumab bind the tumor cell cannot be killed. So by inhibiting PD-L1 the tumor can be Durvalumab killed Hormonal Therapies Drug MOA Uses Dose Tamoxifen Blocks Estrogen receptor (ER). Hormones bind to ER to promote cancer Breast 20-40mg OD growth so by tamoxifen binding, hormones cannot bind. Cancer