Detail of > 128-13-2
- CAS Number:
- 128-13-2
- Name:
Ursodeoxycholic acid
- Formula:
- C24H40O4
- Molecular Structure:

- Synonyms:
- (4R)-4-[(3R,5S,7S,8R,9S,10R,13R,14S,17R)-3,7-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoate;Cholan-24-oic acid, 3,7-dihydroxy-, (3-.alpha.,5-.beta., 7-.beta.)-;Cholan-24-oic acid,3,7-dihydroxy-,(3R,5a,- 7a)-;UDCA;5.beta.-Chol-24-oic acid-3.alpha., 7.beta.-diol;Arsacol;Ursochol;Antigall;Urso (TN);Ursodiol;Antigall (TN);Actigall;Urso;Litursol;Deursil;Desocol;Ursodeoxycholic acid (JP14);Delursan;Ursodiol (USP);deoxy-;Urso Deoxy Cholic Acid;7beta-Hydroxylithocholic acid;Ursodeoxycholoc acid;
- Molecular Weight:
- 392.58 .
- EINECS:
- 204-879-3
- Density:
- 1.128 g/cm3
- Melting Point:
- 203-204 °C(lit.)
- Boiling Point:
- 547.1 °C at 760 mmHg
- Flash Point:
- 298.8 °C
- Solubility:
- practically insoluble in water
- Appearance:
- white crystalline powder
- Hazard Symbols:
Xi- Risk Codes:
- 36/37/38
- Safety:
- 24/25-36-26Details
- Deleted CAS:
- 80225-86-1|50809-41-1
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Reference
- Purification of bile acids for medical use
- Purification of bile acids for medical use. (Tokyo Tanabe Co., Ltd., Japan). Jpn. Kokai Tokkyo Koho JP 58113202 A2 6 Jul 1983 Showa, 4 pp. (Japanese). (Japan). CODEN: JKXXAF. CLASS: IC: C08B037-00. APPLICATION: JP 81-209605 28 Dec 1981. DOCUMENT TYPE: Patent CA Section: 63 (Pharmaceuticals) Crude chenodeoxycholic acid (I) [474-25-9], ursodeoxycholic acid [128-13-2] and 3a-hydroxy-7-ketocholanic acid [28332-54-9] for medical use are purified by fractionation with org. solvents (sec-Bu alc. [78-92-2], tert-amyl alc. [75-85-4], n-hexyl alc. [111-27-3], 2-ethylhexyl alc. [104-76-7] and n-octyl alc. [111-87-5]). As an example, 300 g I (94% pure) was dissolved in n-hexyl alc. (3 L), treated with 3.12 g NaOH in 6.In this article, certain chemicals are used. Some of their cas registry numbers are 111-87-5 and 75-85-4 2 L H2O and the mixt. was stirred at room temp. for 5 min. The upper layer was treated with 1.56 g NaOH in 6.2 L H2O, the mixt. was stirred for 5 min and the org. phase was sepd., washed with water and treated with 31.2 g NaOH in 6.2 L H2O while stirring. The bottom layer then was sepd., concd. and treated with 0.1N H2SO4 to form a ppt., which was crystd. with EtOAc to give cryst. I with 99.9% purity. A 85% yield was obtained. .
- b-Endorphin-like immunoreactivity and VIP release in various loading tests in normal subjects and patients with duodenal ulcer
- b-Endorphin-like immunoreactivity and VIP release in various loading tests in normal subjects and patients with duodenal ulcer. Matsumura, M.; Tomita, S.; Saito, S.; Yamanoi, A.; Yamamoto, S.; Mori, H. (Sch. Med., Tokushima Univ., Tokushima 770, Japan). Gut Pept. Ulcer, Proc. Hiroshima Symp., 2nd, Meeting Date 1982, 335-41. Edited by: Miyoshi, Akima. Biomed. Res. Found.: Tokyo, Japan. (English) 1983. CODEN: 51DSA5. DOCUMENT TYPE: Conference CA Section: 2 (Mammalian Hormones) Section cross-reference(s): 14 The effects of various test materials on plasma b-endorphin [60617-12-1]-like immunoreactivity (b-EpLI) and VIP [37221-79-7] were studied in normal subjects and patients with duodenal ulcer. Plasma b-EpLI and VIP were measured by radioimmunoassay after extn. by the acid-acetone method. Fasting plasma concns. of b-EpLI and VIP were 36.6 pg/mL and 86 pg/mL, resp., and no differences were obsd. between sexes. The plasma b-EpLI and VIP levels were within normal range in the majority of patients with peptic ulcer. 81-24-3 and 37221-79-7 are cas registry numbers of chemicals which are used as reagents here. The oral administration of ursodeoxycholic acid (UDCA) [128-13-2] increased plasma b-EpLI from 25.3 to 107.7 pg/mL, and plasma VIP from 41.3 to 71.3 pg/mL, after 30 min. The intraduodenal infusion of 115 mL of 0.1N HCl over 10 min increased plasma b-EpLI (from 30.4 to 54.3 pg/mL) and plasma VIP levels (from 41.3 to 145.0 pg/mL) at 10 min after the start of the infusion. However, the oral administration of UDCA and duodenal acidification had no effect on plasma b-EpLI and VIP levels in patients with duodenal ulcer. The perifusion expt. demonstrated that the releases of b-EpLI and VIP from human duodenal mucosa into the perifusate were markedly stimulated by the perifusion of the soln. of pH 2 or 1 mM taurocholic acid [81-24-3]. Thus, b-EpLI and VIP release is stimulated by duodenal acidification and bile salt may participate, at least in part, in the postprandial release of b-EpLI and VIP probably from the gastrointestinal tract. .
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