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Details

Stereochemistry ACHIRAL
Molecular Formula C6H6O4.Pt.2H3N
Molecular Weight 371.254
Optical Activity NONE
Defined Stereocenters 0 / 0
E/Z Centers 0
Charge 0

SHOW SMILES / InChI
Structure of CARBOPLATIN

SMILES

N.N.[Pt++].[O-]C(=O)C1(CCC1)C([O-])=O

InChI

InChIKey=OLESAACUTLOWQZ-UHFFFAOYSA-L
InChI=1S/C6H8O4.2H3N.Pt/c7-4(8)6(5(9)10)2-1-3-6;;;/h1-3H2,(H,7,8)(H,9,10);2*1H3;/q;;;+2/p-2

HIDE SMILES / InChI

Molecular Formula C6H6O4
Molecular Weight 142.1094
Charge -2
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Molecular Formula Pt
Molecular Weight 195.084
Charge 2
Count
MOL RATIO 1 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Molecular Formula H3N
Molecular Weight 17.0305
Charge 0
Count
MOL RATIO 2 MOL RATIO (average)
Stereochemistry ACHIRAL
Additional Stereochemistry No
Defined Stereocenters 0 / 0
E/Z Centers 0
Optical Activity NONE

Description

Carboplatin is an organoplatinum compound that possesses antineoplastic activity. Carboplatin is an intravenously administered platinum coordination complex and alkylating agent, which is used as a chemotherapeutic agent for the treatment of various cancers, mainly of advanced ovarian. Carboplatin is indicated for the palliative treatment of patients with ovarian carcinoma recurrent after prior chemotherapy, including patients who have been previously treated with cisplatin. In addition this drug can be used to treat others cancers. Carboplatin therapy is associated with a low rate of transient serum aminotransferase elevations and with rare instances of clinically apparent liver injury. Carboplatin, like cisplatin, produces predominantly interstrand DNA cross-links rather than DNA-protein cross-links. This effect is apparently cell-cycle nonspecific. The aquation of carboplatin, which is thought to produce the active species, occurs at a slower rate than in the case of cisplatin. Despite this difference, it appears that both carboplatin and cisplatin induce equal numbers of drug-DNA cross-links, causing equivalent lesions and biological effects.

Approval Year

Targets

Primary TargetPharmacologyConditionPotency

Conditions

ConditionModalityTargetsHighest PhaseProduct
Primary
CARBOPLATIN

Cmax

ValueDoseCo-administeredAnalytePopulation
38.99 μg/mL
375 mg/m² single, intravenous
CARBOPLATIN plasma
Homo sapiens

AUC

ValueDoseCo-administeredAnalytePopulation
197.71 μg × h/mL
375 mg/m² single, intravenous
CARBOPLATIN plasma
Homo sapiens

T1/2

ValueDoseCo-administeredAnalytePopulation
39.81 h
375 mg/m² single, intravenous
CARBOPLATIN plasma
Homo sapiens

Funbound

ValueDoseCo-administeredAnalytePopulation
100%
CARBOPLATIN plasma
Homo sapiens

Doses

AEs

Overview

OverviewOther

Drug as perpetrator​

Drug as victim

PubMed

Patents

Sample Use Guides

In Vivo Use Guide
Single-Agent Therapy: Carboplatin injection, as a single agent, has been shown to be effective in patients with recurrent ovarian carcinoma at a dosage of 360 mg/m2 IV on day 1 every 4 weeks. In general, however, single intermittent courses of carboplatin should not be repeated until the neutrophil count is at least 2,000 and the platelet count is at least 100,000. Combination Therapy with Cyclophosphamide: In the chemotherapy of advanced ovarian cancer, an effective combination for previously untreated patients consists of: Carboplatin―300 mg/m2 IV on day 1 every 4 weeks for 6 cycles. Cyclophosphamide―600 mg/m2 IV on day 1 every 4 weeks for 6 cycles.
Route of Administration: Intravenous
In Vitro Use Guide
Ovarian cancer cell lines (n=36) were treated with carboplatin, cisplatin, paclitaxel, or carboplatin-paclitaxel (CPTX). For each cell line, IC(50) levels were quantified and pre-treatment gene expression analyses were performed. Drug dilutions initially consisted of 1.5-fold serial dilutions from a maximum concentration of 100 μℳ. The cells were incubated with the drug for 72 h to ensure all cell lines underwent a minimum of two doublings. It was found, that characterisation of gene expression signatures in ovarian cancer (OVCA) patients may be useful for characterisng responses to treatment and also in developing an understanding of the biology that drives clinical outcome and survival. Furthermore, it was identified BAD, APC/C, and CREB was key players in the cytotoxicity of carboplatin, cisplatin, and paclitaxel in OVCA cell lines, and was suggested that targeted therapies against regulators of these proteins may be worthy of study in chemoresistant OVCAs.
Substance Class Chemical
Record UNII
BG3F62OND5
Record Status Validated (UNII)
Record Version