81968-76-5

Basic information

• Product Name: METHYL 4-HYDROXYADAMANTAN-1-CARBOXYLATE
• Synonyms: METHYL 4-HYDROXYADAMANTAN-1-CARBOXYLATE
• CAS NO: 81968-76-5
• Molecular Formula: C₁₂H₁₈O₃
• Molecular Weight: 210.26952
• Mol File: 81968-76-5.mol
• Article Data: 8

Chemical Properties

• Appearance: /
• CAS DataBase Reference: METHYL 4-HYDROXYADAMANTAN-1-CARBOXYLATE(CAS DataBase Reference)
• NIST Chemistry Reference: METHYL 4-HYDROXYADAMANTAN-1-CARBOXYLATE(81968-76-5)
• EPA Substance Registry System: METHYL 4-HYDROXYADAMANTAN-1-CARBOXYLATE(81968-76-5)

Safety Data

• Hazardous Substances Data: 81968-76-5(Hazardous Substances Data)

Upstream product

• 186581-53-3 diazomethane 
• 828-51-3 1-Adamantanecarboxylic acid 
• 112185-86-1 (1S,3R,4S,5S)-4-(4-Nitro-benzenesulfonyloxy)-adamantane-1-carboxylic acid methyl ester 
• 56674-88-5 methyl 4-oxoadamantane-1-carboxylate 
• 67-56-1 methanol 
• 81968-77-6 4-hydroxyadamantane-1-carboxylic acid 
• 56674-87-4 4-oxoadamantane-1-carboxylic acid 

Downstream Products

• 121706-24-9 C₁₇⁽¹⁴⁾CH₂₂O₄S 
• 56674-88-5 methyl 4-oxoadamantane-1-carboxylate 
• 81968-77-6 4-hydroxyadamantane-1-carboxylic acid 
• 41163-64-8 4e-hydroxy-1-adamantanecarboxylic acid 

Relevant articles and documents

Discovery and optimization of adamantane carboxylic acid derivatives as potent diacylglycerol acyltransferase 1 inhibitors for the potential treatment of obesity and diabetes

Abstract We have developed a series of adamantane carboxylic acid derivatives exhibiting potent diacylglycerol acyltransferase 1 (DGAT1) inhibitory activities. Optimization of the series led to the discovery of E-adamantane carboxylic acid compound 43c, which showed excellent in vitro activity with an IC50 value of 5 nM against human and mouse DGAT1, also good druggability as well as microsomal stability and safety profiles such as hERG, CYP and cytotoxicity. Compound 43c significantly reduced plasma triglyceride levels in vivo (in rodents and zebrafish) and also showed bodyweight gain reduction and glucose area under curve (AUC) lowering efficacy in diet-induced obesity (DIO) mice.

CARBAMATE AND UREA INHIBITORS OF 11BETA-HYDROXYSTEROID DEHYDROGENASE 1

This invention relates to novel compounds of the invention pharmaceutically acceptable salts thereof, and pharmaceutical compositions thereof, which are useful for the therapeutic treatment of diseases associated with the modulation or inhibition of 11β-HSD1 in mammals. The invention further relates to pharmaceutical compositions of the novel compounds and methods for their use in the reduction or control of the production of cortisol in a cell or the inhibition of the conversion of cortisone to cortisol in a cell.

Nucleophilic substitution induced by electron transfer at the bridgehead of polycyclic alkanes: Competition between polar and radical pathways

A series of 2,5(or 1,4)-dihaloadamantanes (4 and 5, X = Y = halogens) and 9,10-dihalotriptycenes (7, X = Y = halogens) as well as two 5-halo (X) adamantan-2-ones (6, Y = O,X = Br and I) have been treated with Me3SnLi in THF in the absence and presence of tert-butylamine (TBA) and dicyclohexylphosphine (DCHP). The product distributions of these reactions have been established by 13C and 119Sn NMR spectroscopy, vapor-phase chromatographic analyses, and GC/MS. The former compounds (4 and 5) appear to react exclusively by a free-radical chain process (SRN1 mechanism) to yield tin substitution products. By contrast, the triptycenes react predominantly by a polar mechanism initiated by the formation of a carbanion. In the case of the halo ketones (6, Y = O,X = Br and I), a mechanistic divergence of the reaction was unexpectedly encountered. Whereas the bromo ketone provides the substitution product (6, Y = O,X = SnMe3) in good yield (ca. 75%), apparently by a radical pathway, the iodo ketone yields a fragmentation product (ca. 95% yield) by a polar mechanism. This mechanistic switch highlights the importance of the electronegativity of the leaving group as well as substituent-induced electron delocalization as molecular factors governing the competition between radical and polar pathways.