4649-12-1

Basic information

• Product Name: 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine
• Synonyms: 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine;2-(1H-Pyrrolo[2,3-b]pyridin-3-yl)ethanaMine;1H-Pyrrolo(2,3-B)pyridine-3-ethanaMine 7-AzatryptaMine
• CAS NO: 4649-12-1
• Molecular Formula: C₉H₁₁N₃
• Molecular Weight: 161.20374
• Mol File: 4649-12-1.mol
• Article Data: 13

Chemical Properties

• Boiling Point: 358.4°Cat760mmHg
• Flash Point: 197.9°C
• Appearance: white powders
• Density: 1.225g/cm³
• Vapor Pressure: 2.56E-05mmHg at 25°C
• Refractive Index: 1.679
• Storage Temp.: under inert gas (nitrogen or Argon) at 2–8 °C
• PKA: 10.17±0.10(Predicted)
• CAS DataBase Reference: 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine(CAS DataBase Reference)
• NIST Chemistry Reference: 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine(4649-12-1)
• EPA Substance Registry System: 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine(4649-12-1)

Safety Data

• Hazardous Substances Data: 4649-12-1(Hazardous Substances Data)

Usage

General Description

2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine is a chemical compound with the molecular formula C11H15N3. It belongs to the class of ethanamines and contains a bicyclic structure. 2-(2,9-diazabicyclo[4.3.0]nona-2,4,7,10-tetraen-7-yl)ethanamine is a type of amine and is commonly used in organic synthesis and medicinal chemistry. It has potential applications in the pharmaceutical industry as a building block for the synthesis of various drugs and biologically active molecules. The compound's specific structure and reactivity make it a valuable tool in the development of new therapeutic agents and research into the biological activity of certain substances.

InChI:InChI=1/C9H11N3/c10-4-3-7-6-12-9-8(7)2-1-5-11-9/h1-2,5-6H,3-4,10H2,(H,11,12)

Upstream product

• 4414-87-3 1H-Pyrrolo[2,3-b]pyridin-3-yl-acetonitrile 
• 49758-35-2 (S)-2-amino-3-(1H-pyrrolo[2,3-b]pyridin-3-yl)propanoic acid 
• 271-63-6 7-Azaindole 
• 56-45-1 L-serin 
• 83393-47-9 2-chloro-1-(1H-pyrrolo[2,3-b]pyridin-3-yl)ethan-1-one 
• 183208-29-9 3-(2-nitroethyl)-1H-pyrrolo[2,3-b]pyridine 
• 183208-28-8 3-(2-nitroethenyl)-1H-7-aza-indole 
• 4649-09-6 1H-pyrrolo[2,3-b]pyridin-3-carbaldehyde 
• 90929-74-1 3-(2-Chloro-ethyl)-1H-pyrrolo[2,3-b]pyridine 
• 214604-08-7 3-(2-Iodo-ethyl)-1H-pyrrolo[2,3-b]pyridine 
• 7664-41-7 ammonia 
• 5654-92-2 7-azagramine 
• 7303-50-6 7-azatryptophan 

Downstream Products

• 950888-57-0 C₁₅H₁₄N₄O₂ 
• 895168-35-1 3-methoxy-N-[2-(1H-pyrrolo[2,3-b]pyridin-3-yl)ethyl]benzamide 
• 1354893-21-2 6,7,8,9-tetrahydro-5H-pyrrolo[2,3-b:5,4-c']dipyridine 
• 895168-37-3 8-(3-methoxyphenyl)-6,7,8,9-tetrahydro-5H-pyrido[4′,3′:4,5]pyrrolo[2,3-b]pyridine 

Relevant articles and documents

ONO-8430506: A Novel Autotaxin Inhibitor That Enhances the Antitumor Effect of Paclitaxel in a Breast Cancer Model

Lysophosphatidic acid (LPA) is a bioactive lipid mediator that elicits a number of biological functions, including smooth muscle contraction, cell motility, proliferation, and morphological change. LPA is endogenously produced by autotaxin (ATX) from extracellular lysophosphatidylcholine (LPC) in plasma. Herein, we report our medicinal chemistry effort to identify a novel and highly potent ATX inhibitor, ONO-8430506 (20), with good oral availability. To enhance the enzymatic ATX inhibitory activity, we designed several compounds by structurally comparing our hit compound with the endogenous ligand LPC. Further optimization to improve the pharmacokinetic profile and enhance the ATX inhibitory activity in human plasma resulted in the identification of ONO-8430506 (20), which enhanced the antitumor effect of paclitaxel in a breast cancer model.

Virtual screening-driven discovery of dual 5-HT6/5-HT2A receptor ligands with pro-cognitive properties

A virtual screening campaign aimed at finding structurally new compounds active at 5-HT6R provided a set of candidates. Among those, one structure, 4-(5-{[(2-{5-fluoro-1H-pyrrolo[2,3-b]pyridin-3-yl}ethyl)amino]methyl}furan-2-yl)phenol (1, 5-HT6R Ki = 91 nM), was selected as a hit for further optimization. As expected, the chemical scaffold of selected compound was significantly different from all the serotonin receptor ligands published to date. Synthetic efforts, supported by molecular modelling, provided 43 compounds representing different substitution patterns. The derivative 42, 4-(5-{[(2-{5-fluoro-1H-pyrrolo[2,3-b]pyridin-3-yl}ethyl)amino]methyl}furan-2-yl)phenol (5-HT6R Ki = 25, 5-HT2AR Ki = 32 nM), was selected as a lead and showed a good brain/plasma concentration profile, and it reversed phencyclidine-induced memory impairment. Considering the unique activity profile, the obtained series might be a good starting point for the development of a novel antipsychotic or antidepressant with pro-cognitive properties.

Characterization of the properties of a selective, orally bioavailable autotaxin inhibitor in preclinical models of advanced stages of liver fibrosis

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.