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Cisplatin

Pt(NH3)2Cl2 inorganic

Properties

StateSolid
ColorYellow
SolubilitySlightly soluble in water (2.5 g/L); soluble in DMF and DMSO
Melting Point270 °C (decomposes)

About Cisplatin

Cisplatin is a square-planar Pt(II) d⁸ complex where the geometry of two ammine and two chloride ligands at 90° to each other is the entire reason the molecule cures testicular cancer and the trans isomer doesn't. Inside a cell, the chloride ligands hydrolyze (the cytoplasmic [Cl⁻] of ~4 mM is far below the 100 mM blood plasma level that keeps the prodrug intact in the bloodstream) to give cis-[Pt(NH3)2(H2O)2]²⁺, which then reacts with N7 of guanine in DNA. Because the two reactive Pt sites are cis, the platinum bridges two adjacent guanines on the same strand, almost always in 5'-GG-3' or 5'-AG-3' contexts — the 1,2-intrastrand crosslink kinks the helix by about 35–40°, displaces the minor groove, and recruits HMG-domain proteins that block lesion bypass and trigger apoptosis. Transplatin can't form the same lesion because its leaving groups are 180° apart. Barnett Rosenberg discovered the activity in 1965 by accident: he was running an experiment with platinum electrodes in NH4Cl-buffered E. coli culture and noticed the bacteria stopped dividing but kept elongating into filaments. The platinum was etching off the electrodes and forming cis-[Pt(NH3)2Cl2] in situ — a tiny amount, but enough to inhibit cell division. FDA approval came in 1978, and cisplatin combination therapy still cures over 95% of testicular cancer cases that have not metastasized to brain. Carboplatin (1989) and oxaliplatin (2002) are second- and third-generation analogs designed to reduce the nephrotoxicity that limits cisplatin dosing.

Where you'll encounter it

If you walk into an oncology pharmacy compounding room, cisplatin is one of the cytotoxics you'll see being prepared in a Class II Type B2 biosafety cabinet, because aerosolized platinum compounds cross skin and trigger severe sensitization. Bench biochemists use it as the standard 'kink-the-DNA' tool for studying nucleotide-excision-repair machinery, XPA recognition, and HMGB1 binding. In coordination-chemistry labs it's still the textbook example for explaining the trans effect — the chloride ligands have a much higher trans-influence than ammonia, which is why the synthesis from K2[PtCl4] proceeds cleanly to the cis isomer if you start by adding NH3 first.

Common Uses

  • First-line chemotherapy for non-seminomatous testicular germ-cell tumors via BEP regimen (bleomycin/etoposide/cisplatin)
  • Induction therapy for advanced ovarian, bladder, and head-and-neck squamous-cell carcinomas in combination protocols
  • Concurrent chemoradiotherapy for cervical and nasopharyngeal carcinoma to enhance radiosensitization
  • Reference compound for benchmarking new platinum-based antitumor agent development in medicinal inorganic chemistry
  • Mechanistic probe for studying nucleotide-excision-repair (NER) pathway recognition of bulky DNA adducts
  • Substrate for HMGB1 and XPA protein-binding assays that probe lesion-recognition specificity
  • Teaching example for the trans-effect ordering and isomer-selective synthesis from K2[PtCl4]
  • Component of intraperitoneal chemotherapy regimens for ovarian cancer following cytoreductive surgery

Safety Information

Cytotoxic chemotherapy drug — handle only in negative-pressure compounding pharmacies with HEPA-filtered Class II BSCs and chemo-rated PPE per USP 800. NIOSH lists it on the Hazardous Drug List (Group 1: antineoplastic). GHS H300+H310+H330 (fatal by oral, dermal, and inhalation routes), H340 (mutagenic), H350 (carcinogenic, IARC Group 2A 'probably carcinogenic to humans'), H360 (reproductive toxicity), H372 (kidney damage). Dose-limiting clinical toxicities are nephrotoxicity (proximal-tubule damage starting around 50 mg/m²), peripheral neuropathy (cumulative-dose-dependent above 300 mg/m²), and ototoxicity (irreversible high-frequency hearing loss). Spill response: use chemo-spill kit; chlorine-bleach inactivation is contraindicated because bleach can release toxic platinum species. Standard protocol is sodium thiosulfate decontamination, which reduces Pt(II) to less reactive thiosulfate complexes.

This safety summary is for educational reference only and may not be complete. It is not a substitute for Safety Data Sheets (SDS), medical advice, or professional chemical safety guidance. Always consult appropriate SDS and qualified professionals before handling chemicals.

Constituent Elements

Frequently Asked Questions

What is the molar mass of cisplatin?
cis-[Pt(NH3)2Cl2] is 300.045 g/mol: platinum at 195.084, two ammonias contributing 34.062 (2 × N at 14.007 + 6 × H at 1.008), and two chlorides at 70.906. The clinical dose is calculated by body surface area (typically 50–100 mg/m² per cycle), so for a 1.7 m² adult that's 85–170 mg of compound.
Why is only the cis isomer therapeutically active?
The cytotoxic lesion is a 1,2-intrastrand crosslink between adjacent guanine N7 atoms on the same DNA strand — the two Pt-N(guanine) bonds need to be ~3 Å apart, which only fits if the leaving groups (and therefore the new bonds) start out cis to each other. Transplatin has its chlorides 180° apart, so the best it can manage is a 1,3-intrastrand or interstrand crosslink, neither of which kinks DNA the same way or recruits HMGB1 proteins that block repair. Transplatin has been studied extensively but consistently fails clinically.
How does cisplatin cause kidney damage?
After IV infusion, cisplatin accumulates in renal proximal tubule cells through OCT2 (organic cation transporter 2). Inside the tubule cells, it forms DNA adducts and depletes glutathione, triggering apoptosis of the tubule epithelium. Clinically that shows up as a rise in serum creatinine and a drop in glomerular filtration around day 3–5 after infusion. The standard prevention is aggressive saline hydration (3 L over 24 hours) and mannitol diuresis, which dilute the drug at the tubule and shorten its dwell time. Amifostine and sodium thiosulfate are sometimes added as nephroprotective agents.