Systematic (IUPAC) name
Clinical data
Trade names Paraplatin
  • US: D (Evidence of risk)
Legal status
  • (Prescription only)
Routes of
Pharmacokinetic data
Bioavailability complete
Protein binding Very low
Biological half-life 1.1-2 hours
Excretion renal
CAS Registry Number  Y
ATC code L01
PubChem CID:
DrugBank  Y
ChemSpider  Y
Chemical data
Formula C6H12N2O4Pt
Molecular mass 371.249 g/mol

Carboplatin, or cis-diammine(1,1-cyclobutanedicarboxylato)platinum(II) (trade names Paraplatin and Paraplatin-AQ) is a health system.[3]


  • Side-effects 1
  • Chemistry 2
  • Mechanism of action 3
  • Dose 4
  • History 5
  • Current events 6
  • See also 7
  • References 8
  • Additional references 9
  • External links 10


Relative to cisplatin, the greatest benefit of carboplatin is its reduced side effects, particularly the elimination of nephrotoxic effects. Nausea and vomiting are less severe and more easily controlled.

The main drawback of carboplatin is its myelosuppressive effect. This causes the antibiotics.

Carboplatin is less potent than cisplatin; depending on the strain of cancer, carboplatin may only be 1/8 to 1/45 as effective. The clinical standard of dosage of carboplatin is usually a 4:1 ratio compared to cisplatin; that is, for a dose that usually requires a particular dose of cisplatin, four times as much carboplatin is needed to achieve the same effectiveness. The stable property of carboplatin is a mixed blessing: once uptake of the drug occurs, its retention half-life is considerably longer than cisplatin, but it is also this inertness that causes carboplatin to go right through the human body, and up to 90% of the carboplatin given can be recovered in urine.


In terms of its structure, carboplatin differs from cisplatin in that it has a bidentate dicarboxylate (the ligand is CycloButane DiCarboxylic Acid, CBDCA) in place of the two chloride ligand, which are the leaving groups in cisplatin. For this reason, "CBDCA" is sometimes used in the medical literature as an abbreviation referring to carboplatin. Carboplatin exhibits lower reactivity and slower DNA binding kinetics, although it forms the same reaction products in vitro at equivalent doses with cisplatin. Unlike cisplatin, carboplatin may be susceptible to alternative mechanisms. Some results show that cisplatin and carboplatin cause different morphological changes in MCF-7 cell lines while exerting their cytotoxic behaviour.[4] The diminished reactivity limits protein-carboplatin complexes, which are excreted. The lower excretion rate of carboplatin means that more is retained in the body, and hence its effects are longer lasting (a retention half-life of 30 hours for carboplatin, compared to 1.5-3.6 hours in the case of cisplatin).

Mechanism of action

Two theories exist to explain the molecular mechanism of action of carboplatin with DNA:

  • Aquation, or the like-cisplatin hypothesis.
  • Activation, or the unlike-cisplatin hypothesis.

The former is more accepted owing to the similarity of the leaving groups with its predecessor cisplatin, while the latter hypothesis envisages a biological activation mechanism to release the active Pt2+ species.


Calvert's formula is used to calculate the dose of carboplatin. It takes under consideration the creatinine clearance and the desired area under curve. [5]


Carboplatin was discovered at Michigan State University,[6] and developed at the Institute of Cancer Research in London. Bristol-Myers Squibb gained Food and Drug Administration (FDA) approval for carboplatin, under the brand name Paraplatin, in March 1989. Starting in October 2004, generic versions of the drug became available.

Current events

A recent study in mutant mice suggests that in the subset of women with breast cancer due to BRCA1 and BRCA2 genes (these cause a variety of familial breast cancer) carboplatin may be as much as 20 times more effective than the usual breast cancer treatments.[7] However, similar data in humans has not yet been shown.

Carboplatin has also been used to treat testicular cancer patients with stage 1 seminoma. Recent research indicates that this treatment is more effective and has fewer side effects than adjuvant radiotherapy.[8][9][10] Also, when compared to radiotherapy, it is far more effective at preventing a second testicular cancer developing in the other testicle.[11]

See also


  1. ^ Wheate NJ, Walker S, Craig GE, Oun R (September 2010). "The status of platinum anticancer drugs in the clinic and in clinical trials".  
  2. ^ Apps, M. G., Choi, E. H. Y., Wheate, N. J. (2015). "The state-of-play and future of platinum drugs". Endocrine-related Cancer 22 (4): 219–233.  
  3. ^ "WHO Model List of EssentialMedicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014. 
  4. ^ Natarajan G, Malathi R, Holler E (November 1999). "Increased DNA-binding activity of cis-1,1-cyclobutanedicarboxylatodiammineplatinum(II) (carboplatin) in the presence of nucleophiles and human breast cancer MCF-7 cell cytoplasmic extracts: activation theory revisited".  
  5. ^
  6. ^ "Discovery to Market: Fact Sheet". 
  7. ^ Henderson, Mark (May 1, 2006). "Lung cancer drug may fight breast tumour in women". Times Online. 
  8. ^
  9. ^ "Testicular cancer drug effective". BBC News. 22 July 2005. 
  10. ^ Rose, David (October 6, 2008). "Chemotherapy drug, carboplatin, ‘is safer cure for testicular cancer’". The Times. 
  11. ^ Nelson, Roxanne (June 10, 2008). "Carboplatin as Effective as Radiation in Preventing Relapse in Testicular Cancer". Medscape Medical News. 

Additional references

  • Natarajan G, Malathi R, Holler E (November 1999). "Increased DNA-binding activity of cis-1,1-cyclobutanedicarboxylatodiammineplatinum(II) (carboplatin) in the presence of nucleophiles and human breast cancer MCF-7 cell cytoplasmic extracts: activation theory revisited". Biochem. Pharmacol. 58 (10): 1625–9.  
  • Knox RJ, Friedlos F, Lydall DA, Roberts JJ (April 1986). "Mechanism of cytotoxicity of anticancer platinum drugs: evidence that cis-diamminedichloroplatinum(II) and cis-diammine-(1,1-cyclobutanedicarboxylato)platinum(II) differ only in the kinetics of their interaction with DNA". Cancer Res. 46 (4 Pt 2): 1972–9.  
  • Canetta R, Rozencweig M, Carter SK (September 1985). "Carboplatin: the clinical spectrum to date". Cancer Treat. Rev. 12 (Suppl A): 125–36.  
  • Overbeck TL, Knight JM, Beck DJ (April 1996). "A comparison of the genotoxic effects of carboplatin and cisplatin in Escherichia coli". Mutat. Res. 362 (3): 249–59.  
  • Schnurr B, Gust R (August 2002). "Investigations on the decomposition of carboplatin in infusion solutions". Mikrochimica Acta 140 (1–2): 69–76.  
  • Yang XL, Wang AH (September 1999). "Structural studies of atom-specific anticancer drugs acting on DNA". Pharmacol. Ther. 83 (3): 181–215.  
  • Travis LB, Holowaty EJ, Bergfeldt K; et al. (February 1999). "Risk of leukemia after platinum-based chemotherapy for ovarian cancer". N. Engl. J. Med. 340 (5): 351–7.  

External links

  • MedlinePlus page on carboplatin
  • Carboplatin Dose / Creatinine Clearence Calculator