1392136-43-4

Basic information

• Product Name: Verdinexor (KPT-335)
• Synonyms: Z)-3-(3-(3,5-bis(trifluoroMethyl)phenyl)-1H-1,2,4-triazol-1-yl)-N'-(pyridin-;KPT-335;Verdinexor;Verdinexor(KPT-335);(2Z)-3-[3-[3,5-bis(trifluoromethyl)phenyl]-1H-1,2,4-triazol-1-yl]- 2-propenoic acid-2-(2-pyridinyl)hydrazide;(2Z)-3-(3-(3,5-Bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)-N -(pyridin-2-yl)prop-2-enehydrazide Verdinexor(KPT-335);(KPT335)(Z)-3-(3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)-N'-(pyridin-2-yl)acrylohydrazide
• CAS NO: 1392136-43-4
• Molecular Formula: C₁₈H₁₂F₆N₆O
• Molecular Weight: 442.3178992
• EINECS: -0
• Product Categories: API;Inhibitors
• Mol File: 1392136-43-4.mol
• Article Data: 1

Chemical Properties

• Appearance: /
• Density: 1.49±0.1 g/cm3(Predicted)
• Solubility: ≥44.2 mg/mL in DMSO; insoluble in H2O; ≥2.31 mg/mL in EtOH with ultrasonic
• PKA: 10.04±0.43(Predicted)
• CAS DataBase Reference: Verdinexor (KPT-335)(CAS DataBase Reference)
• NIST Chemistry Reference: Verdinexor (KPT-335)(1392136-43-4)
• EPA Substance Registry System: Verdinexor (KPT-335)(1392136-43-4)

Safety Data

• Hazardous Substances Data: 1392136-43-4(Hazardous Substances Data)

Usage

Uses

Verdinexor is a potent and selective SINE inhibitor, shown to be effective in treating influenza A virus infection in mice and ferret models.

Biological Activity

verdinexor (kpt-335) is a potent and selective inhibitor of nuclear export [1].nuclear export (sine) is mainly mediated by exportin 1 (xpo1) and mediates specific proteins out of the nucleus, which plays an important role in the regulation of proliferation and the cell cycle [2].verdinexor (kpt-335) is a potent and selective sine inhibitor that acts as an antiviral drug. in a549 cells inoculated with the influenza a and b virus, verdinexor effectively inhibited the replication of the influenza a and b virus strains tested. verdinexor (1 μm) caused the accumulation of vrnps in the nuclei and altered the localization of viral ns1. also, verdinexor increased nuclear negative-sense vrna by 56.6-fold and significantly reduced cytoplasmic negative-sense vrna, which suggested that verdinexor blocked vrnp nuclear export. in 293t cells, verdinexor inhibited xpo1-nep binding [1].in mice infected with influenza virus a, verdinexor significantly reduced lung influenza virus a titers. verdinexor also reduced the expression of proinflammatory cytokines tumor necrosis factor alpha, interleukin-6, interleukin-1β and gamma interferon. in mice infected with a lethal dose, verdinexor inhibited virus penetration of the respiratory tract and virus spread in the lungs [1]. in companion dogs with b- and t-cell lymphomas, verdinexor showed potent cytotoxic activity [2].

references

[1]. perwitasari o, johnson s, yan x, et al. verdinexor, a novel selective inhibitor of nuclear export, reduces influenza a virus replication in vitro and in vivo. j virol, 2014, 88(17): 10228-10243.[2]. gravina gl, senapedis w, mccauley d, et al. nucleo-cytoplasmic transport as a therapeutic target of cancer. j hematol oncol, 2014, 7: 85.

Upstream product

• 317319-15-6 3,5-bis(trifluoromethyl)benzothioamide 
• 27126-93-8 3,5-bis(trifluoromethyl)benzonitrile 
• 4930-98-7 pyrid-2-ylhydrazine 
• 1388842-44-1 (Z)-3-(3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)acrylic acid 
• 1333152-22-9 (Z)-isopropyl 3-(3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazol-1-yl)acrylate 
• 1333154-10-1 3-(3,5-bis(trifluoromethyl)phenyl)-1H-1,2,4-triazole 

Relevant articles and documents

HYDRAZIDE CONTAINING NUCLEAR TRANSPORT MODULATORS AND USES THEREOF

The invention generally relates to nuclear transport modulators, e.g., CRM1 inhibitors, and more particularly to a compound represented by structural formula (I): or a pharmaceutically acceptable salt thereof, wherein the values and alternative values for the variables are as defined and described herein. The invention also includes the synthesis and use of a compound of structural formula I, or a pharmaceutically acceptable salt or composition thereof, e.g., in the treatment, modulation and/or prevention of physiological conditions associated with CRM1 activity.