26130-02-9

Basic information

• Product Name: Frentizole
• Synonyms: Frentizole;1-(6-Methoxybenzothiazol-2-yl)-3-phenylurea;Lilly-53616;Frenazole;N-[6-Methoxybenzo[d]thiazol-2-yl]-N'-phenylurea
• CAS NO: 26130-02-9
• Molecular Formula: C₁₅H₁₃N₃O₂S
• Molecular Weight: 299.35
• Mol File: 26130-02-9.mol
• Article Data: 3

Chemical Properties

• Boiling Point: °Cat760mmHg
• Flash Point: °C
• Appearance: /
• Density: 1.42g/cm³
• Refractive Index: 1.752
• PKA: 7.02±0.70(Predicted)
• CAS DataBase Reference: Frentizole(CAS DataBase Reference)
• NIST Chemistry Reference: Frentizole(26130-02-9)
• EPA Substance Registry System: Frentizole(26130-02-9)

Safety Data

• Hazardous Substances Data: 26130-02-9(Hazardous Substances Data)

Usage

Uses

Immunoregulator.

InChI:InChI=1/C15H13N3O2S/c1-20-11-7-8-12-13(9-11)21-15(17-12)18-14(19)16-10-5-3-2-4-6-10/h2-9H,1H3,(H2,16,17,18,19)

Upstream product

• 1747-60-0 6-methoxybenzothiazol-2-ylamine 
• 103-71-9 phenyl isocyanate 
• 945404-21-7 N-(6-methoxybenzo[d]thiazol-2-yl)-1H-imidazole-1-carboxamide 
• 62-53-3 aniline 

Downstream Products

• 58668-52-3 1-(6-hydroxybenzo[d]thiazol-2-yl)-3-phenylurea 

Relevant articles and documents

Molecular Iodine-Promoted [3 + 2] Oxidative Cyclization for the Synthesis of Heteroarene-Fused [1,2,4] Thiadiazoles/Selenadiazoles

Two new classes of heteroarene-fused [1,2,4]thiadiazole and [1,2,4]selenadiazole are synthesized through the iodine-mediated [3 + 2] oxidative cyclization of 2-aminoheteroarenes and isothiocyanates/isoselenocyanates. This oxidative [3 + 2] annulation stra

6-Benzothiazolyl ureas, thioureas and guanidines are potent inhibitors of ABAD/17-HSD10 and potential drugs for Alzheimer's disease treatment: Design, synthesis and in vitro evaluation

Background: The mitochondrial enzyme amyloid beta-binding alcohol dehydrogenase (ABAD) also known as 17-hydroxysteroid dehydrogenase type 10 (17-HSD10) has been connected with the pathogenesis of Alzheimer's disease (AD). ABAD/17-HSD10 is a binding site for the amyloid-beta peptide (A) inside the mitochondrial matrix where it exacerbates A toxicity. Interaction between these two proteins triggers a series of events leading to mitochondrial dysfunction as seen in AD. Methods: As ABAD’s enzymatic activity is required for mediating A toxicity, its inhibition presents a promising strategy for AD treatment. In this study, a series of new benzothiazolylurea analogues have been prepared and evaluated in vitro for their potency to inhibit ABAD/17-HSD10 enzymatic activity. The most potent compounds have also been tested for their cytotoxic properties and their ability to permeate through blood-brain barrier has been predicted. To explain the structure-activity relationship QSAR and pharmacophore studies have been performed. Results and Conclusion: Compound 12 was identified being the most promising hit compound with good inhibitory activity (IC50 = 3.06 ± 0.40 M) and acceptable cytotoxicity profile comparable to the parent compound of frentizole. The satisfactory physical-chemical properties suggesting its capability to permeate through BBB make compound 12 a novel lead structure for further development and biological assessment.