1640972-35-5

Basic information

• Product Name: Tofacitinib Impurity 6
• Synonyms: Tofacitinib Impurity 6;Tofacitinib Impurity 39;5,6-Dihydro CP-690550;3-((3R,4R)-3-((6,7-dihydro-5H-pyrrolo[2,3-d]pyrimidin-4-yl)(methyl)amino)-4-methylpiperidin-1-yl)-3-oxopropanenitrile;Tofacitinib Related Compound 21;(3R,4R)-3-[(6,7-Dihydro-5H-pyrrolo[2,3-d]pyrimidin-4-yl)methylamino]-4-methyl-β-oxo-1-piperidinepropanenitrile
• CAS NO: 1640972-35-5
• Molecular Formula: C16H22N6O
• Molecular Weight: 314.38548
• Mol File: 1640972-35-5.mol
• Article Data: 1

Chemical Properties

• Boiling Point: 583.2±50.0 °C(Predicted)
• Appearance: /
• Density: 1.239±0.06 g/cm3(Predicted)
• Storage Temp.: -20°C Freezer
• Solubility: DMSO (Slightly), Methanol (Slightly)
• PKA: 6.04±0.60(Predicted)
• CAS DataBase Reference: Tofacitinib Impurity 6(CAS DataBase Reference)
• NIST Chemistry Reference: Tofacitinib Impurity 6(1640972-35-5)
• EPA Substance Registry System: Tofacitinib Impurity 6(1640972-35-5)

Safety Data

• Hazardous Substances Data: 1640972-35-5(Hazardous Substances Data)

Usage

Description

Tofacitinib Impurity 6 is a chemical compound that is an impurity of Tofacitinib, a pyrrolo[2,3-d]pyrimidine derivative, which acts as a Janus kinase inhibitor. It is used for the treatment of rheumatoid arthritis and other inflammatory conditions.

Uses

Used in Pharmaceutical Industry:
Tofacitinib Impurity 6 is used as a reference material for the development and quality control of Tofacitinib, ensuring the purity and efficacy of the drug for the treatment of rheumatoid arthritis and other inflammatory conditions.

Upstream product

• 372-09-8 cyanoacetic acid 

Relevant articles and documents

Tofacitinib Is a Mechanism-Based Inactivator of Cytochrome P450 3A4

Tofacitinib (TFT) is an oral JAK inhibitor which has been approved for the treatment of moderately and severely active rheumatoid arthritis. TFT was found to show concentration-, time-, and NADPH-dependent inhibition of CYP3A4, and irreversibility of the inactivation was also observed. Incubation (40 min, 37 °C) of recombinant CYP3A4 with TFT at 200 μM resulted in >70% loss of CYP3A4 activity. Estimated kinact and KI were 0.037 min-1 and 93.2 μM, respectively. GSH and superoxide dismutase/catalase revealed minor or little protection against the CYP3A4 inactivation. Furthermore, ketoconazole attenuated TFT-mediated CYP3A4 inactivation. Epoxide and α-keto-aldehyde intermediates of TFT were trapped and characterized in microsomal incubations, respectively. The aldehyde intermediate is believed to be the key for the enzyme inactivation. Multiple P450 enzymes, including CYPs2C19, 3A4, 2D6, and 1A2, participated in the metabolism of TFT to the epoxide, while the formation of the aldehyde was mainly catalyzed by CYP3A4. In conclusion, TFT was proven to be a mechanism-based inactivator of CYP3A4.