101030-72-2

Basic information

• Product Name: N-(4-hydroxyphenyl)-3-methylbut-2-enamide
• CAS NO: 101030-72-2
• Molecular Formula: C₁₁H₁₃NO₂
• Molecular Weight: 191.2264
• Mol File: 101030-72-2.mol

Chemical Properties

• Boiling Point: 400.7°C at 760 mmHg
• Flash Point: 196.2°C
• Density: 1.166g/cm³
• Vapor Pressure: 5.38E-07mmHg at 25°C
• Refractive Index: 1.601
• CAS DataBase Reference: N-(4-hydroxyphenyl)-3-methylbut-2-enamide(CAS DataBase Reference)
• NIST Chemistry Reference: N-(4-hydroxyphenyl)-3-methylbut-2-enamide(101030-72-2)
• EPA Substance Registry System: N-(4-hydroxyphenyl)-3-methylbut-2-enamide(101030-72-2)

Safety Data

• Hazardous Substances Data: 101030-72-2(Hazardous Substances Data)

Upstream product

• 541-47-9 3-Methylbutenoic acid 
• 104-94-9 4-methoxy-aniline 
• 109729-85-3 N-(4-methoxyphenyl)-3-methyl-2-butenamide 
• 123-30-8 4-amino-phenol 
• 3350-78-5 3,3-Dimethylacryloyl chloride 

Relevant articles and documents

A COMPOUND AS A THYROID HORMONE BETA RECEPTOR AGONIST AND USE THEREOF

Provided herein is a compound as a thyroid hormone β receptor agonist and use thereof. It further relates to a pharmaceutical composition comprising the compound. The compound or the pharmaceutical composition can be used in the manufacture of a medicament for preventing, treating or alleviating diseases regulated by thyroid hormone β receptors, especially in the manufacture of a medicament for treating non-alcoholic fatty liver disease.

Analysis of chain length, substitution patterns, and unsaturation of AM-404 derivatives as 20S proteasome stimulators

Proteasome-mediated degradation of proteins is a vital cellular process and is performed by the ubiquitin-dependent proteasome system (UPS) and the ubiquitin-independent proteasome system (UIPS). While both systems are necessary to maintain healthy cell function, many disease states are characterized by reduced activity of the UPS, and the UIPS cannot by itself maintain proper protein levels. It has been suggested that the 20S core particle (20S CP), the isoform of the proteasome in the UIPS that can degrade proteins without a ubiquitin tag, can be stimulated with a small molecule to assist the 20S CP to accept and hydrolyze substrates more rapidly. Several small molecule stimulators of the 20S CP have since been discovered, including AM-404, an arachidonic acid derivative. AM-404 has previously been shown to inhibit fatty acid amide hydrolase activity. We wished to evaluate what structural components of AM-404 are required to stimulate the 20S CP with the long-term goal of using this information to design a stimulator with better drug-like qualities. We synthesized numerous derivatives of AM-404, varying the chain length, substitutions, and degree of unsaturation. Through this endeavor, we obtained several molecules capable of stimulating the 20S CP to various degrees. We discovered that though chain length is important, the presence of a cis-alkene in a specific location in the aliphatic chain has the greatest impact on the ability to stimulate the 20S CP. Two of the derivatives maintain modest stimulatory activity, and have improved toxicity over AM-404.

INHIBITORS OF DIHYDROCERAMIDE DESATURASE FOR TREATING DISEASE

Disclosed herein are dihydroceramide desaturase 1 (Des1) inhibitor compounds and compositions, which are useful in the treatment of diseases, such as metabolic, cardiovascular, fibrotic, autoimmune/chronic inflammatory diseases, cystic fibrosis, various cancers, neurodegenerative diseases, lipid storage disorders, and ischemia/reperfusion injury, where inhibition of Des1 is expected to be therapeutic to a patient. Methods of inhibition of Des1 activity in a human or animal subject are also provided.

Fenretinide derivatives act as disrupters of interactions of serum retinol binding protein (sRBP) with transthyretin and the sRBP receptor

Serum retinol binding protein (sRBP) is released from the liver as a complex with transthyretin (TTR), a process under the control of dietary retinol. Elevated levels of sRBP may be involved in inhibiting cellular responses to insulin and in generating first insulin resistance and then type 2 diabetes, offering a new target for therapeutic attack for these conditions. A series of retinoid analogues were synthesized and examined for their binding to sRBP and their ability to disrupt the sRBP-TTR and sRBP-sRBP receptor interactions. A number inhibit the sRBP-TTR and sRBP-sRBP receptor interactions as well as or better than Fenretinide (FEN), presenting a potential novel dual mechanism of action and perhaps offering a new therapeutic intervention against type 2 diabetes and its development. Shortening the chain length of the FEN derivative substantially abolished binding to sRBP, indicating that the strength of the interaction lies in the polyene chain region. Differences in potency against the sRBP-TTR and sRBP-sRBP receptor interactions suggest variant effects of the compounds on the two loops of sRBP guarding the entrance of the binding pocket that are responsible for these two protein-protein interactions.

Aluminium chloride-catalyzed intermolecular vs intramolecular friedel-crafts reaction of acrylanilides and 3-chloropropanamides

3-Phenylpropionanilide (4a) is obtained in a yield of 89% from acrylanilide by the treatment with AlCl3/ benzene, compared with a yield of 39% by the 1,4-conjugate addition of phenyllithium. The formation of 4a indicated that an intermolecular Friedel-Crafts reaction occurred, rather than the relatively more facile intramolecular ring cyclization, and provided a more efficient route than a conjugate addition of phenyllithium for the preparation of 3-phenylpropionanilide and its derivatives. Although the methoxy group is an activator of the nucleophilic substitution, introduction of a methoxy substituent at N-phenyl did not increase the competitive capability of the intramolecular cyclization because of AlCl3-catalyzed demethylation to form the ArOAlCl2 complex which decreased the availability of the π-electron in the N-phenyl aromatic system.