 Cisplatin or carboplatin -Platin

Cisplatin: binds to DNA, forming DNA adducts (crosslinking of DNA). This leads to cell-
cycle arrest, DNA-damage recognition and repair, and programmed cell
death/apoptosis. (Alkylating agent).
- Nephrotoxicity, neurotoxicity, and ototoxicity.

Cyclophosphamides, Ifosfamide, Melphalan, Lomustine have similar MOA of Cisplatin.

- Induces beneficial immunomodulatory effects in adaptive immunotherapy

 Etoposide (topoisomerase II inhibitor):

Ternary complex with topoisomerase II and DNA and prevent resulting in the break DNA
strand  Accumulation of DNA breaks and cell death. Cells in the S and G2 phases of
the cell cycle are most sensitive to etoposide.
- Bone marrow suppression

 Doxorubicin (anthracycline antibiotics - adriamycin):

Intercalation of DNA Cause breaks in DNA strands by inhibiting topoisomerase II
- Cardiotoxicity

 Mitomycin alkylating agent that cross-links DNA.

- Renal damage

 Bleomycin
 Chelates Cu or Fe.
 DNA- bleomycin-Fe(II) complex appears to undergo oxidation to bleomycin-Fe(III);
the liberated electrons react with oxygen to form superoxide or hydroxide radicals,
which in turn attack the phosphodiester bonds of the DNA, resulting in strand
breakage, chain scission and inhibits repair.
- Pulmonary fibrosis
- Raynaud's phenomenon

 Vinblastine, vincristine (Mitotic inhibitor/Antimicrotubule):

Binds tubulin, thereby inhibiting the assembly of microtubules M phase specific cell
cycle Arrest.
- Gastrointestinal problems

 Paclitaxel (Mitotic inhibitor):

Alter the dynamic equilibrium of tubulin-microtubule, it stabilizes microtubules and, as
a result, interferes with the normal breakdown of microtubules during cell division.
- Ovarian damage
- Leuprolide, a GnRH analog prevent ovarian damage.

 Bevacizumab/Avastin  Anti-VEGF, Ab’s that targets the ligand. -Zumab

- Bevacizumab worsen conditions like coronary artery disease or peripheral artery
disease.
- Bowel perforation.
Antiendrogens:
1) Progesterone derivative Cyproterone.
Competes with testosterone, inhibit testicular androgen production.
2) Non-steroidal antiandrogens Flutamide and bicalutamide -lutamide

Irinotecan and topotecan causes single strand breaks in DNA by affecting topoisomerase I
-tecan