1229652-21-4 Usage
Uses
Different sources of media describe the Uses of 1229652-21-4 differently. You can refer to the following data:
1. HA 150 is a selective boronic acid-based inhibitor of autotaxin. Studies show that adminstration of HA 150 in mice results in rapid decrease of the lipid mediator lysophosphatidic acid (LPA) in the circulation. These findings suggest that HA 150 may provide useful therapeutic strategy in treating disorders associated with vascular development, inflammation, fibrotic disease, and tumor progression.
2. HA130 is a selective boronic acid-based inhibitor of autotaxin. Studies show that adminstration of HA130 in mice results in rapid decrease of the lipid mediator lysophosphatidic acid (LPA) in the circulation. These findings suggest that HA 150 may provide useful therapeutic strategy in treating disorders associated with vascular development, inflammation, fibrotic disease, and tumor progression.
Check Digit Verification of cas no
The CAS Registry Mumber 1229652-21-4 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,2,2,9,6,5 and 2 respectively; the second part has 2 digits, 2 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 1229652-21:
(9*1)+(8*2)+(7*2)+(6*9)+(5*6)+(4*5)+(3*2)+(2*2)+(1*1)=154
154 % 10 = 4
So 1229652-21-4 is a valid CAS Registry Number.
1229652-21-4Relevant articles and documents
Discovery and optimization of boronic acid based inhibitors of Autotaxin
Albers, Harald M. H. G.,Van Meeteren, Laurens A.,Egan, David A.,Van Tilburg, Erica W.,Moolenaar, Wouter H.,Ovaa, Huib
experimental part, p. 4958 - 4967 (2010/09/10)
Autotaxin (ATX) is an extracellular enzyme that hydrolyzes lysophosphatidylcholine (LPC) to produce the lipid mediator lysophosphatidic acid (LPA). The ATX-LPA signaling axis has been implicated in diverse physiological and pathological processes, including vascular development, inflammation, fibrotic disease, and tumor progression. Therefore, targeting ATX with small molecule inhibitors is an attractive therapeutic strategy. We recently reported that 2,4-thiazolidinediones inhibit ATX activity in the micromolar range. Interestingly, inhibitory potency was dramatically increased by introduction of a boronic acid moiety, designed to target the active site threonine in ATX. Here we report on the discovery and further optimization of boronic acid based ATX inhibitors. The most potent of these compounds inhibits ATX-mediated LPC hydrolysis in the nanomolar range (IC50 = 6 nM). The finding that ATX can be targeted by boronic acids may aid the development of ATX inhibitors for therapeutic use.
