Abiplatin;Biocisplatinum;Briplatin;Carboquone;Cis Pt II;Cismaplat;Cisplatine;Cisplatyl;Citoplationo;Lederplatin;Neoplatin;Plastin;Platamine;Platiblastin;Platidiam;Platinex;Platinol;Platinol-AQ;Platinoxan;Randa;

CACP;Cis-DDP;Cis-Diaminedichloroplatinum;Cis-Diamminedichloroplatinum;CPDC;CPDD;DDP;DDPT;Diamminedichloroplatinum;Platinum Ammine Chloride;Platinum Ammonium Chloride;Platinum Diamine Dichloride;Trans-DDP;Trans-Diaminedichloroplatinum;Trans-Diamminedichloroplatinum;Trans-Dichlorodiammine Platinum;Trans-Platinumdiammine Dichloride;

Cisplatin, cisplatinum or cis-diamminedichloroplatinum(II) (CDDP) is a platinum-based chemotherapy drug used to treat various types of cancers, including sarcomas, some carcinomas (e.g. small cell lung cancer, and ovarian cancer), lymphomas and germ cell tumors. It was the first member of its class, which now also includes carboplatin and oxaliplatin.

• App pharmaceuticals llc
• Bedford laboratories div ben venue laboratories inc
• Bristol myers co
• Pharmachemie bv
• Teva parenteral medicines inc

• APP Pharmaceuticals
• APPD
• Baxter International Inc.
• Bedford Labs
• Ben Venue Laboratories Inc.
• Bristol-Myers Squibb Co.
• Mead Johnson and Co.
• Pharmachemie BV
• Sicor Pharmaceuticals
• Teva Pharmaceutical Industries Ltd.

Synthesis Reference	Not Available
General Reference	Not Available

Type	small molecule

Classes

Inorganic Ions and Gases

Substructures

Cations Inorganic Ions and Gases

Cancer 癌症;

Indication	For the treatment of metastatic testicular tumors, metastatic ovarian tumors and advanced bladder cancer.
Pharmacodynamics	Cisplatin is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death.
Mechanism of action	Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.
Absorption	Not Available
Volume of distribution	Not Available
Protein binding	Greater than 90%.
Metabolism	Not Available
Route of elimination	The parent compound, cisplatin, is excreted in the urine. Although small amounts of platinum are present in the bile and large intestine after administration of cisplatin, the fecal excretion of platinum appears to be insignificant.
Half life	20-30 minutes
Clearance	15 – 16 L/h/m2 [After infusions of 100 mg/m2.]
Toxicity	Not Available
Affected organisms	Humans and other mammals
Pathways	Not Available

Properties
State	solid
Experimental Properties	Property Value Source melting point 270 dec °C PhysProp water solubility 2530 mg/L (at 25 °C) AMUNDSEN,AR & STERN,EW (1982) logP -2.19 HANSCH,C ET AL. (1995)
Predicted Properties	Property Value Source logP 0.041 ChemAxon pKa (strongest basic) 5.06 ChemAxon physiological charge 0 ChemAxon hydrogen acceptor count 2 ChemAxon hydrogen donor count 2 ChemAxon polar surface area 52.04 ChemAxon rotatable bond count 0 ChemAxon refractivity 22.84 ChemAxon polarizability 10.31 ChemAxon

Drug	Interaction
Amikacin	Increased risk of nephrotoxicity
Bendamustine	Increases toxicity through pharmacodynamic synergism. Additive myelosuppression.
Bumetanide	Increased ototoxicity
Cabazitaxel	Platinum derivatives such as cisplatin may enhance the myelosuppressive effect of taxane derivatives such as cabazitaxel. Administer taxane derivative before platinum derivative when given as sequential infusions to limit toxicity.Administer paclitaxel before cisplatin, when given as sequential infusions, to limit toxicity. Problems associated with other taxane/platinum combinations are possible, although unsubstantiated. Administering the taxane derivative before the platinum derivative seems prudent.
Docetaxel	Platinum derivatives such as cisplatin may enhance the myelosuppressive effect of taxane derivatives such as docetaxel. Administer taxane derivative before platinum derivative when given as sequential infusions to limit toxicity. Administer paclitaxel before cisplatin, when given as sequential infusions, to limit toxicity. Problems associated with other taxane/platinum combinations are possible, although unsubstantiated. Administering the taxane derivative before the platinum derivative seems prudent.
Ethacrynic acid	Increased ototoxicity
Fosphenytoin	The antineoplasic agent decreases the effect of hydantoin
Furosemide	Increased ototoxicity
Gentamicin	Increased risk of nephrotoxicity
Leflunomide	Immunosuppressants such as cisplatin may enhance the adverse/toxic effect of leflunomide. Specifically, the risk for hematologic toxicity such as pancytopenia, agranulocytosis, and/or thrombocytopenia may be increased. Consider eliminating the use of a leflunomide loading dose in patients who are receiving other immunosuppressants in order to reduce the risk for serious adverse events such as hematologic toxicity. Also, patients receiving both leflunomide and another immunosuppressive medication should be monitored for bone marrow suppression at least monthly throughout the duration of concurrent therapy.
Methotrexate	Cisplatin increases methotrexate toxicity
Natalizumab	Immunosuppressants such as cisplatin may enhance the adverse/toxic effect of natalizumab. Specifically, the risk of concurrent infection may be increased. Patients receiving natalizumab should not use concurrent immunosuppressants, and patients receiving chronic corticosteroids prior to natalizumab should be tapered off of steroids prior to starting natalizumab.
Netilmicin	Increased risk of nephrotoxicity
Paclitaxel	Cisplatin increases the effect and toxicity of paclitaxel
Phenytoin	The antineoplasic agent decreases the effect of hydantoin
Pimecrolimus	Pimecrolimus may enhance the adverse/toxic effect of immunosuppressants such as cisplatin. Avoid use of pimecrolimus cream in patients receiving immunosuppressants.
Roflumilast	Roflumilast may enhance the immunosuppressive effect of immunosuppressants such as cisplatin. The Canadian roflumilast product monograph recommends avoiding concurrent use of roflumilast with any immunosuppressant medications due to the antiinflammatory/immune altering effects of roflumilast and the lack of relevant clinical experience with such use. Of note, this recommendation to avoid concurrent use does not apply to either inhaled corticosteroids (which have much more limited systemic immune-suppressing actions) or short-term systemic corticosteroid use. U.S. prescribing information does not contain this warning; but it appears prudent to avoid this combination when possible.
Tacrolimus	Additive renal impairment may occur during concomitant therapy with aminoglycosides such as Cisplatin. Use caution during concomitant therapy.
Tobramycin	Increased risk of nephrotoxicity
Topotecan	Administration of Topotecan after Cisplatin therapy may increase the risk of hematologic toxicity, such as neutropenia and/or thrombocytopenia. A dose adjustment may be required or the sequence of administration reversed.
Trastuzumab	Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events.

• Echinacea should be used with caution, if at all, in patients receiving therapeutic immunosuppressants. Monitor for reduced efficacy of the immunosuppressant during concomitant use.