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Carboplatin

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(Treatment for antineoplastic medication)

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Carboplatin is a platinum coordination compound that is used as a cancer chemotherapeutic agent.

The chemical name for carboplatin is platinum, diammine [1,1-cyclobutane-dicarboxylato(2-)-0,0']-,(SP-4-2).

Carboplatin is a crystalline powder with the molecular formula of C 6 H 12 N 2 O 4 Pt and a molecular weight of 371.25. It is soluble in water at a rate of approximately 14 mg/mL, and the pH of a 1% solution is 5-7. It is virtually insoluble in ethanol, acetone, and dimethylacetamide.

Chemical structural formula:

Type of Drug:

Carboplatin is a platinum chemotherapy drug that belongs to a general group of drugs known as alkylating agents. It is used to treat ovarian, lungs, and other cancers.

How Drug Works:

Carboplatin stops the growth of cancer cells, causing the cells to die.

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

The former is more accepted owing to the similarity of the leaving groups with its predecessor cisplatin, while the latter hypothesis envisages a biologically activation mechanism to release the active Pt 2+ species.

Side Effects:

The largest benefit of using carboplatin over cisplatin is the reduction of side effects; particularly the elimination of cisplatin's nephrotoxic effects. This is due in part to the added stability of carboplatin in the bloodstream, which prevents proteins from binding to it. This in turn reduces the amount of these protein-carboplatin complexes to be 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).

There are no known ototoxic effects from carboplatin. Nausea and vomiting are less severe and more easily controlled, compared to the incessant vomiting and antiperistalsis that some patients using cisplatin may experience. Carboplatin has also proven effective in some strains of cancer that may not be susceptible to cisplatin, including germ-line cell, small and non-small cell lung, ovary, and bladder cancers, as well as acute leukemia .

The main drawback of carboplatin is its myelosuppressive effects. This causes the blood cell and platelet output of bone marrow in the body to decrease quite dramatically, sometimes as low as 10% of its usual production levels. The nadir of this myelosuppression usually occurs 21-28 days after the first treatment, after which the blood cell and platelet levels in the blood begin to stabilize, often coming close to its pre-carboplatin levels. This decrease in white blood cells ( neutropenia ) causes many complications, most notably infection by opportunistic organisms. This necessitates readmission to hospital and treatment with antibiotics .

The potency of carboplatin is also something to be desired compared to cisplatin. Depending on which strain of cancer, carboplatin can be over 8 to 45 times less effective compared to cisplatin. 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 more carboplatin is needed to achieve the same effectiveness. The stable property of carboplatin is a mixed blessing: although once uptake of the drug occurs, its retention half-life is considerably longer than cisplatin, it is also due to 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.

Recent studies have provided a way to increase the effectiveness of carboplatin by first incubating carboplatin in a sodium chloride (NaCl) solution. After 24 hours, an analysis was performed on the solution by separating the compounds by thin-layer chromatography (TLC). The TLC isolated cisplatin, carboplatin, and several platinum bi-products in the solution. Numerous trials were done, and the trend showed that the survival rate of E. coli dropped dramatically as the molarity of the NaCl incubating solution increased. The treated E. coli also showed decreased amounts of alkaline phosphatase, a protein indicator of cellular size. This suggests that as this incubated carboplatin solution was administered to cells, they began to shrink and eventually die; apparently by the same mechanism that cisplatin works.

More Common Side Effects:

Less Common Side Effects:

Rare Side Efects:

REFERENCES

  1. Recommendations for the Safe Handling of Parenteral Antineoplastic Drugs. NIH Publication No. 83-2621. For sale by the Superintendent of Documents, US Government Printing Office, Washington, DC 20402.
  2. AMA Council Report. Guidelines for Handling Parenteral Antineoplastics. JAMA 1985; 253(11):1590-1592.
  3. National Study Commission on Cytotoxic Exposure--Recommendations for Handling Cytotoxic Agents. Available from Louis P. Jeffrey, ScD, Chairman, National Study Commission on Cytotoxic Exposure, Massachusetts College of Pharmacy and Allied Health Sciences, 179 Longwood Avenue, Boston, Massachusetts 02115.
  4. Clinical Oncological Society of Australia. Guidelines and Recommendations for Safe Handling of Antineoplastic Agents. Med J Australia 1983; 1:426-428.
  5. Jones RB, et al: Safe Handling of Chemotherapeutic Agents: A Report from the Mount Sinai Medical Center. CA-A Cancer Journal for Clinicians 1983; (Sept/Oct)258-263.
  6. American Society of Hospital Pharmacists Technical Assistance Bulletin on Handling Cytotoxic and Hazardous Drugs. Am J Hosp Pharm 1990; 47:1033-1049.
  7. Controlling Occupational Exposure to Hazardous Drugs. (OSHA WORK PRACTICE GUIDELINES). Am J Health-Syst Pharm 1995; 52:1669-1685.

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