58584-83-1

Basic information

• Product Name: 2,6-Dichloronicotinoyl chloride
• Synonyms: 2,6-Dichloronicotinoyl chloride;2,6-Dichloropyridine-3-carbonyl chloride;2,6-Dichloronicotinyl Chloride;2,6-Dichloropyridine-3-carbonyl chloride 96%;2,6-Dichloropyridine-3-carboxylic chloride;EOS-62046
• CAS NO: 58584-83-1
• Molecular Formula: C₆H₂Cl₃NO
• Molecular Weight: 210.45
• Product Categories: Building Blocks;C5 to C6;C6 to C7;Chemical Synthesis;Halogenated Heterocycles;Heterocyclic Building Blocks;Pyridines
• Mol File: 58584-83-1.mol
• Article Data: 25

Chemical Properties

• Melting Point: 24-30 °C
• Boiling Point: 72-74 °C(Press: 0.01 Torr)
• Flash Point: 110 °C
• Appearance: /
• Density: 1.582±0.06 g/cm3(Predicted)
• Solubility: Dichloromethane, Ethyl Acetate, Toluene
• PKA: -5.16±0.10(Predicted)
• CAS DataBase Reference: 2,6-Dichloronicotinoyl chloride(CAS DataBase Reference)
• NIST Chemistry Reference: 2,6-Dichloronicotinoyl chloride(58584-83-1)
• EPA Substance Registry System: 2,6-Dichloronicotinoyl chloride(58584-83-1)

Safety Data

• Hazard Codes: C
• Statements: 22-34
• Safety Statements: 26-36/37/39-45
• RIDADR: UN 3261 8/PG 2
• WGK Germany: 3
• Hazardous Substances Data: 58584-83-1(Hazardous Substances Data)

Usage

Uses

2,6-Dichloronicotinyl Chloride is a reactant used in the preparation of semisynthetic derivatives of andrographolide and inhibitors of hepatitis C (HCV) NS5B polymerase.

Upstream product

• 38496-18-3 2,6-dichloropyridine-3-carboxylic acid 

Downstream Products

• 1024035-79-7 (S)-2-(1-(5-(cyclohexylcarbamoyl)-6-(isopentyloxy)pyridin-2-yl)piperidin-3-yl)acetic acid 

Relevant articles and documents

BICYCLIC COMPOUND AND USE THEREOF

The present disclosure relates to a compound derivative containing a 6-7 bicyclic ring and use thereof. The compound according to the present invention can be effectively used in the prevention or treatment of diseases caused by PRMT5 by acting as a PRMT5 inhibitor.

Gut-Restricted Selective Cyclooxygenase-2 (COX-2) Inhibitors for Chemoprevention of Colorectal Cancer

Selective cyclooxygenase (COX)-2 inhibitors have been extensively studied for colorectal cancer (CRC) chemoprevention. Celecoxib has been reported to reduce the incidence of colorectal adenomas and CRC but is also associated with an increased risk of cardiovascular events. Here, we report a series of gut-restricted, selective COX-2 inhibitors characterized by high colonic exposure and minimized systemic exposure. By establishing acute ex vivo 18F-FDG uptake attenuation as an efficacy proxy, we identified a subset of analogues that demonstrated statistically significant in vivo dose-dependent inhibition of adenoma progression and survival extension in an APCmin/+ mouse model. However, in vitro-in vivo correlation analysis showed their chemoprotective effects were driven by residual systemic COX-2 inhibition, rationalizing their less than expected efficacies and highlighting the challenges associated with COX-2-mediated CRC disease chemoprevention.

Discovery of [1,2,4]triazolo[4,3-a]pyridines as potent Smoothened inhibitors targeting the Hedgehog pathway with improved antitumor activity in vivo

Triple-negative breast cancer (TNBC), a subset of breast cancers, have poorer survival than other breast cancer types. Recent studies have demonstrated that the abnormal Hedgehog (Hh) pathway is activated in TNBC and that these treatment-resistant cancers are sensitive to inhibition of the Hh pathway. Smoothened (Smo) protein is a vital constituent in Hh signaling and an attractive drug target. Vismodegib (VIS) is one of the most widely studied Smo inhibitors. But the clinical application of Smo inhibitors is limited to adult patients with BCC and AML, with many side effects. Therefore, it's necessary to develop novel Smo inhibitor with better profiles. Twenty [1,2,4]triazolo[4,3-a]pyridines were designed, synthesized and screened as Smo inhibitors. Four of these novel compounds showed directly bound to Smo protein with stronger binding affinity than VIS. The new compounds showed broad anti-proliferative activity against cancer cell lines in vitro, especially triple-negative breast cancer cells. Mechanistic studies demonstrated that TPB15 markedly induced cell cycle arrest and apoptosis in MDA-MB-468 cells. TPB15 blocked Smo translocation into the cilia and reduced Smo protein and mRNA expression. Furthermore, the expression of the downstream regulatory factor glioma-associated oncogene 1 (Gli1) was significantly inhibited. Finally, TPB15 demonstrated greater anti-tumor activity in our animal models than VIS with lower toxicity. Hence, these results support further optimization of this novel scaffold to develop improved Smo antagonists.