Dabrafenib manufacturers and suppliers in india

Dabrafenib

CAS:: 1195765-45-7

MF:: C23H20F3N5O2S2

MW:: 519.56

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Properties

Melting point:: 214-216oC

Boiling point:: 653.7±65.0 °C(Predicted)

Density: 1.443

storage temp.: -20°C

solubility: Soluble in DMSO (up to 30 mg/ml with warming), or in Ethanol (up to 1 mg/ml with warming).

form: White solid.

pka: 6.62±0.10(Predicted)

color: Off-white

Stability:: Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20°C for up to 3 months.

InChIKey: BFSMGDJOXZAERB-UHFFFAOYSA-N

SMILES: C1(S(NC2=CC=CC(C3=C(C4C=CN=C(N)N=4)SC(C(C)(C)C)=N3)=C2F)(=O)=O)=C(F)C=CC=C1F

Safety Information

Symbol(GHS): GHS08,GHS09

Signal word: Warning

Hazard statements: H361-H411-H400

Precautionary statements: P273-P391-P501-P201-P202-P281-P308+P313-P405-P501

HS Code: 29350090

Use

N-[3-[5-(2-Amino-4-pyrimidinyl)-2-(tert-butyl)-4-thiazolyl]-2-fluorophenyl]-2,6-difluorobenzenesulfonamide is well known as dabrafenib. It is a drug for the treatment of cancers associated with a mutated version of the gene BRAF. Dabrafenib acts as an inhibitor of the associated enzyme B-Raf, which plays a role in the regulation of cell growth. Dabrafenib has clinical activity with a manageable safety profile in clinical trials of phase-I and -II in patients with BRAF(V600)-mutated metastatic melanoma1,2. Its mechanism of action is acted as a Protein Kinase Inhibitor, and Cytochrome P450 3A4 Inducer, and Cytochrome P450 2B6 Inducer, and Cytochrome P450 2C8 Inducer, and Cytochrome P450 2C9 Inducer, and Cytochrome P450 2C19 Inducer, and Organic Anion Transporting Polypeptide 1B1 Inhibitor, and Organic Anion Transporting Polypeptide 1B3 Inhibitor, and Organic Anion Transporter 1 Inhibitor, and Organic Anion Transporter 3 Inhibitor, and Breast Cancer Resistance Protein Inhibitor3,4. It is not indicated for the treatment of patients with wild-type BRAF melanoma or wild-type BRAF NSCLC. MEKINIST is not indicated for the treatment of patients with melanoma who have progressed on prior BRAF-inhibitor therapy5.