1245643-61-1

Basic information

• Product Name: methyl 5-chloro-1H-indole-6-carboxylate
• Synonyms: methyl 5-chloro-1H-indole-6-carboxylate;5-Chloro-indole-6-carboxylic acid Methyl ester
• CAS NO: 1245643-61-1
• Molecular Formula: C10H8ClNO2
• Molecular Weight: 210
• Mol File: 1245643-61-1.mol
• Article Data: 1

Chemical Properties

• Appearance: /
• Storage Temp.: under inert gas (nitrogen or Argon) at 2-8°C
• CAS DataBase Reference: methyl 5-chloro-1H-indole-6-carboxylate(CAS DataBase Reference)
• NIST Chemistry Reference: methyl 5-chloro-1H-indole-6-carboxylate(1245643-61-1)
• EPA Substance Registry System: methyl 5-chloro-1H-indole-6-carboxylate(1245643-61-1)

Safety Data

• HazardClass: IRRITANT
• Hazardous Substances Data: 1245643-61-1(Hazardous Substances Data)

Usage

General Description

Methyl 5-chloro-1H-indole-6-carboxylate is a synthetic chemical compound distinguished by its indole core structure, an aromatic heterocyclic organic compound, and unique functional groups, including a methyl ester and a chlorine atom. The presence of an indole ring provides the molecule with specific properties that can make it useful in various applications, such as in drug development or as a precursor in synthetic chemistry. The chlorine atom attached improves its reactivity, potentially allowing for further chemical modifications. As with any synthetic chemical, handling should be done with standard safety precautions due to possible hazards or negative health impacts.

Upstream product

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Downstream Products

• 1619236-12-2 phenyl 5-chloro-1-methylindoline-6-carbonylcarbamate 

Relevant articles and documents

Identification, optimization, and pharmacology of acylurea GHS-R1a inverse agonists

Ghrelin plays a major physiological role in the control of food intake, and inverse agonists of the ghrelin receptor (GHS-R1a) are widely considered to offer utility as antiobesity agents by lowering the set-point for hunger between meals. We identified an acylurea series of ghrelin modulators from high throughput screening and optimized binding affinity through structure-activity relationship studies. Furthermore, we identified specific substructural changes, which switched partial agonist activity to inverse agonist activity, and optimized physicochemical and DMPK properties to afford the non-CNS penetrant inverse agonist 22 (AZ-GHS-22) and the CNS penetrant inverse agonist 38 (AZ-GHS-38). Free feeding efficacy experiments showed that CNS exposure was necessary to obtain reduced food intake in mice, and it was demonstrated using GHS-R1a null and wild-type mice that this effect operates through a mechanism involving GHS-R1a.