1354893-21-2 Usage
Uses
Used in Pharmaceutical Development:
6,7,8,9-Tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine is used as a ligand for the α7 nicotinic acetylcholine receptor, for its potential role in the development of new drugs to treat neurological and psychiatric disorders. Its partial agonist activity at this receptor suggests it may have therapeutic benefits in conditions where the receptor's function is implicated.
Used in Medicinal Chemistry Research:
In the field of medicinal chemistry, 6,7,8,9-Tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine is used as a starting point for the synthesis of new derivatives. These derivatives are investigated for their enhanced pharmacological properties, potentially leading to the creation of more effective and targeted treatments for various diseases and conditions.
Used in Drug Discovery for Neurological Disorders:
6,7,8,9-Tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine is utilized in drug discovery processes specifically aimed at neurological disorders. Its interaction with the α7 nicotinic acetylcholine receptor makes it a candidate for the development of treatments for conditions such as Alzheimer's disease, schizophrenia, and other cognitive impairments where this receptor plays a significant role.
Used in Drug Discovery for Psychiatric Disorders:
Similarly, in the realm of psychiatric disorders, 6,7,8,9-Tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine is employed in the search for novel therapeutic agents. Its agonist properties at the α7 nicotinic acetylcholine receptor could contribute to the management of symptoms in disorders such as depression, anxiety, and other mood-related conditions.
Used in Synergistic Drug Development:
6,7,8,9-Tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine is also considered for use in synergistic drug development, where it may be combined with other compounds to enhance the overall therapeutic effect. This approach could lead to more effective treatments with fewer side effects, particularly in complex conditions that require multi-target intervention.
Check Digit Verification of cas no
The CAS Registry Mumber 1354893-21-2 includes 10 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 7 digits, 1,3,5,4,8,9 and 3 respectively; the second part has 2 digits, 2 and 1 respectively.
Calculate Digit Verification of CAS Registry Number 1354893-21:
(9*1)+(8*3)+(7*5)+(6*4)+(5*8)+(4*9)+(3*3)+(2*2)+(1*1)=182
182 % 10 = 2
So 1354893-21-2 is a valid CAS Registry Number.
1354893-21-2Relevant articles and documents
Characterization of the properties of a selective, orally bioavailable autotaxin inhibitor in preclinical models of advanced stages of liver fibrosis
Baader, Manuel,Bretschneider, Tom,Broermann, Andre,Rippmann, Joerg F,Stierstorfer, Birgit,Kuttruff, Christian A,Mark, Michael
, p. 693 - 707 (2018)
Background and Purpose: Autotaxin (ATX) is a secreted phospholipase which hydrolyses lysophosphatidylcholine to generate lysophosphatidic acid (LPA). The extracellular signalling molecule LPA exerts its biological actions through activation of six GPCRs expressed in various cell types including fibroblasts. Multiple preclinical studies using knockout animals, LPA receptor antagonists or ATX inhibitors have provided evidence for a potential role of the ATX/LPA axis in tissue fibrosis. Despite growing evidence for a correlation between ATX levels and the degree of fibrosis in chronic liver diseases, including viral hepatitis and hepatocellular carcinoma, the role of ATX in non-alcoholic steatohepatitis (NASH) remains unclear. Experimental Approach: The relevance of ATX in the pathogenesis of liver fibrosis was investigated by oral administration of Ex_31, a selective ATX inhibitor, in a 10?week model of carbon tetrachloride-induced liver injury and in a 14?week model of choline-deficient amino acid-defined diet-induced liver injury in rats. Key Results: Oral administration of Ex_31, a selective ATX inhibitor, at 15?mg·kg?1 twice daily in therapeutic intervention mode resulted in efficient ATX inhibition and more than 95% reduction in plasma LPA levels in both studies. Treatment with Ex_31 had no effect on biomarkers of liver function, inflammation, or fibrosis and did not result in histological improvements in diseased animals. Conclusions and Implications: Our findings question the role of ATX in the pathogenesis of hepatic fibrosis and the potential of small molecule ATX inhibitors for the treatment of patients with NASH and advanced stages of liver fibrosis.
