1452-29-5

Usage

InChI:InChI=1/C24H36O3/c1-15(4-9-22(26)27)19-7-8-20-18-6-5-16-14-17(25)10-12-23(16,2)21(18)11-13-24(19,20)3/h14-15,18-21H,4-13H2,1-3H3,(H,26,27)/t15-,18+,19-,20+,21+,23+,24-/m1/s1

Upstream product

• 110-86-1 pyridine 
• 104825-76-5 4β-bromo-3-oxo-5β-cholan-24-oic acid 
• 1452-33-1 methyl 3-oxo-4-cholenolate 
• 601-57-0 Cholest-4-en-3-one 
• 64-19-7 acetic acid 
• 5255-17-4 3β-hydroxy-5-cholenoic acid 
• 1857-80-3 5α,6β-dibromocholestan-3β-ol 
• 127-09-3 sodium acetate 
• 20231-57-6 methyl 5-cholenoate 
• 1553-56-6 dehydrolithocholic acid 
• 112018-64-1 (R)-4-((5S,8S,9S,10R,13R,14S,17R)-4-Bromo-10,13-dimethyl-3-oxo-hexadecahydro-cyclopenta[a]phenanthren-17-yl)-pentanoic acid methyl ester 
• 1173-32-6 methyl 3-oxo-5β-cholan-24-oate 
• 1249-75-8 methyl lithocholate 
• 434-13-9 Lithocholic acid 

Downstream Products

• 1452-33-1 methyl 3-oxo-4-cholenolate 
• 473462-29-2 24-(benzoyloxy)-4-oxachol-5-en-3-one 
• 473462-28-1 24-(benzoyloxy)-chol-4-en-3-one 
• 1025965-86-9 Benzoic acid (R)-4-[(3R,3aR,5aS,6R,9aS,9bS)-6-(2-carboxy-ethyl)-3a,6-dimethyl-7-oxo-dodecahydro-cyclopenta[a]naphthalen-3-yl]-pentyl ester 
• 1452-33-1 (R)-4-((8S,9S,10R,13R,14S)-10,13-Dimethyl-3-oxo-2,3,6,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)-pentanoic acid methyl ester 
• 20231-57-6 methyl 5-cholenoate 
• 288099-95-6 6-{(4aR,4bS,6aR,7R,9aS,9bS,11aR)-7-[(R)-4-(4-Cyano-benzyloxy)-1-methyl-butyl]-4a,6a-dimethyl-hexadecahydro-indeno[5,4-f]quinolin-1-yl}-hexanoic acid tert-butyl ester 

Relevant academic research and scientific papers

Synthesis of esters of bile acids and avermectin B1

Esters of bile acids and avermectin B1 were obtained for the first time by the reaction of avermectin B1 with bile acid anhydrides.

Synthesis of [3,4-13C2]-enriched bile salts as NMR probes of protein-ligand interactions

Synthetic methodology that allows for incorporation of isotopic carbon at the C-3 and C-4 positions of bile salts is reported. Three [3,4-13C2]-enriched bile salts were synthesized from either deoxycholic or lithocholic acid. The steroid 3α-OH group was oxidized and the A-ring was converted into the Δ4-3-ketone. The C-24 carboxylic acid was next converted into the carbonate group and selectively reduced to the alcohol in the presence of the A-ring enone. Following protection of the 24-OH group, the Δ4-3-ketone was converted into the A-ring enol lactone. Condensation of the enol lactone with [1,2-13C2]-enriched acetyl chloride and subsequent Robinson annulation afforded a [3,4-13C2]-enriched Δ4-3-ketone that was subsequently converted back into a 3α-hydroxy-5β-reduced bile steroid. C-7 hydroxylation, when necessary, was achieved via conversion of the Δ4-3-ketone into the corresponding Δ4,6-dien-3-one, epoxidation of the Δ6-double bond, and hydrogenolysis/hydrogenation of the 5,6-epoxy enone system. The [3,4-13C2]-enriched bile salts were subsequently complexed to human ileal bile acid binding protein (I-BABP), and 1H-13C HSQC spectra were recorded to show the utility of the compounds for investigating the interactions of bile acids with I-BABP.

Synthesis and in vitro biological activity of 4α(2-propenyl)-5α- cholest-24-en-3α-ol: A 24,25-dehydro analog of the hypocholesterolemic agent 4α-(2-propenyl)-5α-cholestan-3α-ol

4α-(2-Propenyl)-5α-cholestan-3α-ol (LY295427) was previously identified from a Chinese hamster ovary (CHO) cell-based low density lipoprotein receptor/luciferase (LDLR/Luc) assay to be a potent transcriptional activator of the LDL receptor promoter in the presence of 25- hydroxycholesterol. To investigate the effect of the 24,25-unsaturation in the D-ring side chain (desmosterol D-ring side chain) on antagonizing the repressing effect of 25-hydroxycholesterol, 4α-(2-propenyl)-5α-cholest-24- en-3α-ol (17), a 24,25-dehydro analog of LY295427, was thus synthesized from lithocholic acid via the formation of 3α-[[(1,1- dimethylethyl)dimethylsilyl]oxy]-4α-(2-propenyl)5α-cholan-24-al (15). Test results showed that 17 had an EC(30) value of 2.6 (max)M, comparable to 2.9 (max)M of LY295427, in the CHO cell-based LDLR/Luc assay in the presence of 25-hydroxycholesterol. Apparently, the built-in 24,25-unsaturation in the D- ring side chain of 17 had added little effect to antagonizing the repressing effect of 25-hydroxycholesterol. In the [1-14C-acetate]cholesterol biosynthesis inhibition assay, 17 at 10 μg/ml (23 μM) has been shown to inhibit the cholesterol biosynthesis in CHO cells by 38% relative to the vehicle control; whereas LY295427 showed no inhibition in the same assay in our previous studies. In contrast to LY295427, the built-in 24,25- unsaturation in the D-ring side chain of 17 has conferred an inhibitory effect on cholesterol biosynthesis in CHO cells. In summary, the observed LDL receptor promoter activity of 17 is related to its ability to prevent 25- hydroxycholesterol from exerting the repressing effect via an undetermined mechanism and, in part, to inhibit the cholesterol biosynthesis.

Regio- and stereo-selective oxidation of steroids using 2,6-dichloropyridine N-oxide catalysed by ruthenium porphyrins

Ruthenium porphyrins catalyse oxygen transfer from 2,6-dichloropyridine N-oxide to steroids with retention of configuration at the asymmetric centre, giving novel steroids.

SYNTHETIC STUDIES ON VITAMIN D ANALOGUES VI. A NEW SYNTHESIS OF 25-HYDROXYCHOLESTEROL FROM LITHOCHOLIC ACID

The conversion of lithocholic acid (1) into 25-hydroxycholesterol (10) via methyl 3β-hydroxy-5-cholenate (6) is described.