Carboplatin

Biological Activity

Carboplatin is a second-generation platinum compound with a broad spectrum of antineoplastic properties. Carboplatin is activated intracellularly to form reactive platinum complexes that bind to nucleophilic groups such as GC-rich sites in DNA, thereby inducing intrastrand and interstrand DNA cross-links, as well as DNA-protein cross-links. Carboplatin possesses tumoricidal activity similar to that of its parent compound, cisplatin, but is more stable and less toxic. Carboplatin is used against some forms of cancer (mainly ovarian carcinoma, lung, head and neck cancers). 

DMSO can inactivate Carboplatin's activity

Product Citations

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  Universitat Freiburg im Breisgau. 2020 Jul.

  Investigation of chemotherapy-induced non-coding RNA expression alterations in clinical breast cancer management
  Carboplatin purchased from AbMole

• 

  Int J Oncol. 2020 Jan;56(1):47-68.

  Circulating non‑coding RNA‑biomarker potential in neoadjuvant chemotherapy of triple negative breast cancer?
  Carboplatin purchased from AbMole

• 

  Cell Cycle. 2018;17(10):1235-1244.

  Apatinib, a novel tyrosine kinase inhibitor, suppresses tumor growth in cervical cancer and synergizes with Paclitaxel.
  Carboplatin purchased from AbMole

• 

  Cell Death Dis. 2018 Feb 12;9(2):213.

  Autophagy mediates glucose starvationinduced glioblastoma cell quiescence and chemoresistance through coordinating cell metabolism, cell cycle, and survival
  Carboplatin purchased from AbMole

Customer Product Validations & Biological Datas

	Source	Cell Cycle (2018 Jul). Figure 5. Carboplatin (Abmole Bioscience)
	Method	cellular proliferation assay
	Cell Lines	SiHa cells
	Concentrations	5 μM
	Incubation Time	-
	Results	However, we found no synergy between Apatinib and cisplatin (CI ranged from 1.149 to 5.647 in SiHa, CI ranged from 0.85 to 1.682 in Hcc94) or carboplatin (CI ranged from 0.669 to 1.402 in SiHa and from 0.955 to 1.206 in Hcc94)

	Source	Cell Death Dis (2018). Figure 3. Carboplatin (Abmole Bioscience)
	Method	Glucose starvation sensitizes glioblastoma cells to chemotherapies
	Cell Lines	U87 and U251 cells
	Concentrations	50 μM
	Incubation Time	5 d
	Results	Treatment with either temozolomide or carboplatin induced about 50 and 80% GBM cell death under normal and glucose starvation conditions, respectively

	Source	Cell Death Dis (2018). Figure 1. Carboplatin (Abmole Bioscience)
	Method	Glucose starvation sensitizes glioblastoma cells to chemotherapies
	Cell Lines	U87 and U251 cells
	Concentrations	50 μM
	Incubation Time	5 d
	Results	The cytotoxic effect was progressive and by day 5, temozolomide or carboplatin treatment caused 40–60% cell loss in U87 and U251 cells. Glucose starvation nearly doubled the cell loss to 70–90%.

	Source	Mol Oncol (2014). Figure 4. Carboplatin
	Method	s.c.
	Cell Lines	Female 6-week-old nude mice
	Concentrations	100 mg/kg
	Incubation Time	5 weeks
	Results	Both carboplatin treatment groups showed significantly reduced tumor burden as compared to the untreated controls from weeks 4 to 10 (P < 0.0001)

Protocol

Cell Experiment
Cell lines	5637 cells
Preparation method	Cells were dosed and incubated with 290 μM carboplatin or 290 μM carboplatin combined with 0.08 μM paclitaxel for 4 h, each including 0.43 μM[14C]carboplatin (106 dpm/ml). After washing, cells were maintained with 14C carboplatin-free culture media. DNA was extracted from cells and converted to graphite and measured by AMS for 14C quantification as previously described.
Concentrations	290 μM
Incubation time	4 h

Animal Experiment
Animal models	Female 6‐week‐old nude mice
Formulation
Dosages	100 mg/kg
Administration	s.c.

Conversion of different model animals based on BSA (Value based on data from FDA Draft Guidelines)

Species	Mouse	Rat	Rabbit	Guinea pig	Hamster	Dog
Weight (kg)	0.02	0.15	1.8	0.4	0.08	10
Body Surface Area (m2)	0.007	0.025	0.15	0.05	0.02	0.5
Km factor	3	6	12	8	5	20

Animal A (mg/kg) = Animal B (mg/kg) multiplied by	Animal B Km
	Animal A Km

For example, to modify the dose of Compound A used for a mouse (20 mg/kg) to a dose based on the BSA for a rat, multiply 20 mg/kg by the K_m factor for a mouse and then divide by the K_m factor for a rat. This calculation results in a rat equivalent dose for Compound A of 10 mg/kg.

Chemical Information

References

[1] Jiang S, et al. Chem Res Toxicol. Paclitaxel Enhances Carboplatin-DNA Adduct Formation and Cytotoxicity.

[2] Moisan F, et al. Mol Oncol. Enhancement of paclitaxel and carboplatin therapies by CCL2 blockade in ovarian cancers.

[3] Matthew D Hall, et al. Cancer Res. Say no to DMSO: dimethylsulfoxide inactivates cisplatin, carboplatin, and other platinum complexes