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Carboplatin: molecular mechanisms of action associated with ...
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Carboplatin , sold under the trade name Paraplatin among others, is a chemotherapy drug used to treat some forms of cancer. These include ovarian cancer, lung cancer, head and neck cancer, brain cancer, and neuroblastoma. This is used by injection into the blood vessels.

Side effects generally occur. Common side effects include low blood cell levels, nausea, and electrolyte problems. Other serious side effects include allergic reactions and an increased risk of other cancers in the future. Use during pregnancy can cause harm to the baby. Carboplatin is present in the platinum-based platelet antineoplastic family and works by disrupting DNA duplication.

Carboplatin was patented in 1972 and approved for medical use in 1986. It is a List of Essential Medicines of the World Health Organization, the most effective and safe drugs needed in the health system. Wholesale costs in developing countries are around 26.49 to 37.37 USD per 450Ã, mg vial. In the United Kingdom that weighed down the National Institute of Health (NIH) around 160 pounds (about 200 USD).


Video Carboplatin



Medical use

Carboplatin is used to treat some forms of cancer. These include ovarian cancer, lung cancer, head and neck cancer, brain cancer, and neuroblastoma. It can be used for some types of testicular cancer but cisplatin is generally more effective.

Maps Carboplatin



Side effects

With regard to cisplatin, the greatest benefit of carboplatin is its diminished side effects, especially the removal of nephrotoxic effects. Nausea and vomiting are lighter and easier to control.

The main drawback of carboplatin is the myelosuppressive effect. This causes blood cells and platelet output from the bone marrow in the body to drop quite drastically, sometimes as low as 10% of the usual production level. Nadir mielosupresi usually occurs 21-28 days after the first treatment, after which blood cells and platelet levels in the blood begin to stabilize, often close to the pre-carboplatin level. This decrease in white blood cells (neutropenia) can cause complications, and is sometimes treated with drugs such as filgrastim. The most important complication of neutropenia is the increased likelihood of infection by opportunistic organisms, requiring patients to reenter hospital and treatment with antibiotics.

Carboplatin is less potent than cisplatin; depending on the cancer strain, carboplatin can only be 1/8 to 1/45 as effective. Clinical standard of carboplatin dose is usually a 4: 1 ratio compared to cisplatin; that is, for doses that typically require a certain dose of cisplatin, four times as much carboplatin is required to achieve the same effectiveness. The stable nature of carboplatin is a blend of the mixture: once the drug uptake occurs, retention of the beak is much longer than cisplatin, but also this inertness that causes carboplatin to penetrate the human body, and up to 90% of carboplatin administered can be recovered in urine.

Carboplatin cancer drug molecule Stock Photo: 283813592 - Alamy
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Chemistry

In terms of its structure, carboplatin differs from cisplatin in that it has a bidentate dicarboxylic (ligand is CycloButane DiCarboxylic Acid, CBDCA) in place of two chloride ligands, which is a leaving group in cisplatin. For this reason, "CBDCA" is sometimes used in medical literature as an abbreviation refers to carboplatin. Carboplatin exhibits lower reactivity and slower DNA binding kinetics, although it forms the same in vitro reaction product at the equivalent dose of cisplatin. Unlike cisplatin, carboplatin may be susceptible to alternative mechanisms. Some results suggest that cisplatin and carboplatin cause different morphological changes in MCF-7 cell pathways when exerting their cytotoxic behavior. The reduced reactivity limits the protein complex-carboplatin, which is excreted. Lower carboplatin excretion rates mean more are retained in the body, and hence their effects are more durable (half-life retention of 30 hours for carboplatin, compared with 1.5-3.6 hours in cisplatin cases).

Carboplatin cancer chemotherapy drug, chemical structure. Atoms ...
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Action mechanism

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

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

The former is more acceptable because of the similarity the group leaves with its predecessor cisplatin, while the latter hypothesis envisages the mechanism of biological activation to release active Pt 2 species.

Kemocarb (Carboplatin) - Fresenius Kabi Egypt
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Dose

The Calvert formula is used to calculate doses of carboplatin. It takes under consideration of creatinine permits and the desired area under the curve.

Thioridazine enhances sensitivity to carboplatin in human head and ...
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History

Carboplatin was found at Michigan State University, and was developed at the Institute of Cancer Research in London. Bristol-Myers Squibb obtained the approval of the Food and Drug Administration (FDA) for carboplatin, under the Paraplatin brand name, in March 1989. Beginning in October 2004, a generic version of the drug was available.

Carboplatin cancer chemotherapy drug, chemical structure. Atoms ...
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Research

Carboplatin has also been used for adjuvant therapy of stage 1 semenomatous testicular cancer. Studies have shown that it is no less effective than adjuvant radiotherapy for this treatment, while having fewer side effects. This leads to adjuvant therapy based on carboplatin which is generally preferred over adjuvant radiotherapy in clinical practice.

Weekly administration of paclitaxel and carboplatin with ...
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See also

  • Cisplatin
  • Dicycloplatin

Carboplatin Cancer Chemotherapy Drug, Chemical Structure Atoms ...
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References


Carboplatin Cancer Chemotherapy Drug, Chemical Structure Atoms ...
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Additional references




External links

  • MedlinePlus page on carboplatin
  • Creatinin Creativity Calculator [sic]

Source of the article : Wikipedia

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