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1252003-15-8

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1252003-15-8 Usage

Definition

ChEBI: A pyridoindole that is 1,2,3,4-tetrahydro-5H-pyrido[4,3-b]indole which is substituted on the tetrahydropyridine nitrogen by a methyl group and on the indole nitrogen by a p-[N-(hydroxy)aminoca bonyl]benzyl group. It is a histone deacetylase 6 (HDAC6) inhibitor that is selective against all the other isozymes (1000-fold) except HDAC8 (57-fold).

Check Digit Verification of cas no

The CAS Registry Mumber 1252003-15-8 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,2,5,2,0,0 and 3 respectively; the second part has 2 digits, 1 and 5 respectively.
Calculate Digit Verification of CAS Registry Number 1252003-15:
(9*1)+(8*2)+(7*5)+(6*2)+(5*0)+(4*0)+(3*3)+(2*1)+(1*5)=88
88 % 10 = 8
So 1252003-15-8 is a valid CAS Registry Number.

1252003-15-8SDS

SAFETY DATA SHEETS

According to Globally Harmonized System of Classification and Labelling of Chemicals (GHS) - Sixth revised edition

Version: 1.0

Creation Date: Aug 16, 2017

Revision Date: Aug 16, 2017

1.Identification

1.1 GHS Product identifier

Product name N-Hydroxy-4-[(2-methyl-1,2,3,4-tetrahydro-5H-pyrido[4,3-b]indol-5 -yl)methyl]benzamide

1.2 Other means of identification

Product number -
Other names Tubastatin-A

1.3 Recommended use of the chemical and restrictions on use

Identified uses For industry use only.
Uses advised against no data available

1.4 Supplier's details

1.5 Emergency phone number

Emergency phone number -
Service hours Monday to Friday, 9am-5pm (Standard time zone: UTC/GMT +8 hours).

More Details:1252003-15-8 SDS

1252003-15-8Relevant articles and documents

HDAC6 inhibitor accelerates wound healing by inhibiting tubulin mediated IL-1β secretion in diabetic mice

Ghosh, Balaram,Goli, Sriharshini,Karnam, Kalyani,Kulkarni, Onkar Prakash,Routholla, Ganesh,Sedmaki, Kavitha,Sharma, Pravesh,Venuganti, Venkata Vamsi Krishna

, (2020/08/06)

Delayed wound healing in diabetes is characterized by sustained activation of inflammasome and increased expression of IL-1β in macrophages. Identification and validation of novel pathways to regulate IL-1β expression will provide therapeutic targets for

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