3199-71-1

Basic information

• Product Name: 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL
• Synonyms: 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL
• CAS NO: 3199-71-1
• Molecular Formula: C9H9ClO
• Molecular Weight: 168.62
• Mol File: 3199-71-1.mol
• Article Data: 9

Chemical Properties

• Boiling Point: 287.3°C at 760 mmHg
• Flash Point: 127.5°C
• Appearance: /
• Density: 1.322g/cm³
• Vapor Pressure: 0.00117mmHg at 25°C
• Refractive Index: 1.622
• CAS DataBase Reference: 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL(CAS DataBase Reference)
• NIST Chemistry Reference: 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL(3199-71-1)
• EPA Substance Registry System: 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL(3199-71-1)

Safety Data

• Hazardous Substances Data: 3199-71-1(Hazardous Substances Data)

Usage

General Description

4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL is a chemical compound with the molecular formula C9H9ClO. It is a chlorinated indenol derivative that is commonly used in the synthesis of pharmaceuticals and agrochemicals. 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL has a bicyclic structure consisting of an indene ring and a chloro-substituted hydroxyl group. It is often employed as an intermediate in the production of various pharmaceuticals and organic compounds due to its versatile reactivity and functional groups. Additionally, 4-CHLORO-2,3-DIHYDRO-1H-INDEN-1-OL has potential applications in organic synthesis and medicinal chemistry due to its structural features and reactivity.

InChI:InChI=1/C9H9ClO/c10-8-3-1-2-7-6(8)4-5-9(7)11/h1-3,9,11H,4-5H2

Upstream product

• 83-33-0 inden-1-one 
• 15115-59-0 4-chloro-2,3-dihydro-1H-inden-1-one 
• 89-98-5 2-chloro-benzaldehyde 
• 30573-88-7 ethyl 3-(2-chlorophenyl)propanoate 
• 24393-51-9 (E)-ethyl 2-chlorocinnamate 
• 1643-28-3 3-(2-chlorophenyl)propanoic acid 

Downstream Products

• 52085-99-1 7-chloro-1H-indene 

Relevant articles and documents

Tetrahydrofuran-Based Transient Receptor Potential Ankyrin 1 (TRPA1) Antagonists: Ligand-Based Discovery, Activity in a Rodent Asthma Model, and Mechanism-of-Action via Cryogenic Electron Microscopy

Transient receptor potential ankyrin 1 (TRPA1) is a nonselective calcium-permeable ion channel highly expressed in the primary sensory neurons functioning as a polymodal sensor for exogenous and endogenous stimuli and has generated widespread interest as a target for inhibition due to its implication in neuropathic pain and respiratory disease. Herein, we describe the optimization of a series of potent, selective, and orally bioavailable TRPA1 small molecule antagonists, leading to the discovery of a novel tetrahydrofuran-based linker. Given the balance of physicochemical properties and strong in vivo target engagement in a rat AITC-induced pain assay, compound 20 was progressed into a guinea pig ovalbumin asthma model where it exhibited significant dose-dependent reduction of inflammatory response. Furthermore, the structure of the TRPA1 channel bound to compound 21 was determined via cryogenic electron microscopy to a resolution of 3 ?, revealing the binding site and mechanism of action for this class of antagonists.

SUBSTITUTED HETEROCYCLIC DERIVATIVES AS GPR AGONISTS AND USES THEREOF

The present invention generally relates to substituted heterocyclic derivatives (the compounds of Formula (I)), processes for their preparation, pharmaceutical compositions containing said compounds, their use as G-protein coupled receptor (GPR) agonists, particularly as GPR40 agonists and methods of using these compounds in the treatment of GPR40 mediated diseases or conditions such as Type 2 diabetes, obesity, dyslipidemia, hyperlipidemia, hypercholesterolemia, and hypertriglyceridemia.

Synthesis and biological evaluation of novel 2,4-diaminoquinazoline derivatives as SMN2 promoter activators for the potential treatment of spinal muscular atrophy

Proximal spinal muscular atrophy (SMA) is an autosomal recessive disorder characterized by death of motor neurons in the spinal cord that is caused by deletion and/or mutation of the survival motor neuron gene (SMN1). Adjacent to SMN1 are a variable number of copies of the SMN2 gene. The two genes essentially differ by a single nucleotide, which causes the majority of the RNA transcripts from SMN2 to lack exon 7. Although both SMN1 and SMN2 encode the same Smn protein amino acid sequence, the loss of SMN1 and incorrect splicing of SMN2 have the consequence that Smn protein levels are insufficient for the survival of motor neurons. The therapeutic goal of our medicinal chemistry effort was to identify small-molecule activators of the SMN2 promoter that, by up-regulating gene transcription, would produce greater quantities of full-length Smn protein. Our initial medicinal chemistry effort explored a series of C5 substituted benzyl ether based 2,4-diaminoquinazoline derivatives that were found to be potent activators of the SMN2 promoter; however, inhibition of DHFR was shown to be an off-target activity that was linked to ATP depletion. We used a structure-guided approach to overcome DHFR inhibition while retaining SMN2 promoter activation. A lead compound 11a was identified as having high potency (EC50 = 4 nM) and 2.3-fold induction of the SMN2 promoter. Compound 11a possessed desirable pharmaceutical properties, including excellent brain exposure and long brain half-life following oral dosing to mice. The piperidine compound 11a up-regulated expression of the mouse SMN gene in NSC-34 cells, a mouse motor neuron hybrid cell line. In type 1 SMA patient fibroblasts, compound 11a induced Smn in a dose-dependent manner when analyzed by immunoblotting and increased the number of intranuclear particles called gems. The compound restored gems numbers in type I SMA patient fibroblasts to levels near unaffected genetic carriers of SMA.