X
1. D2, Pro-vitamin
2. Lumisterol
3. Pro Vitamin D2
4. Pro-vitamin D2
5. Provitamin D 2
1. 57-87-4
2. Provitamin D2
3. Ergosterin
4. Ergosta-5,7,22-trien-3-ol, (3b,22e)-
5. Ergosta-5,7,22e-trien-3beta-ol
6. Z30ray509f
7. Chebi:16933
8. (22e,24s)-24-methylcholesta-5,7,22-trien-3beta-ol
9. (22e)-ergosta-5,7,22-trien-3beta-ol
10. (22e)-ergosta-5,7,22-trien-3.beta.-ol
11. 24-methylcholesta-5,7,22-trien-3beta-ol
12. Ergosta-5,7,22-trien-3beta-ol
13. (3s,9s,10r,13r,14r,17r)-17-[(e,2r,5r)-5,6-dimethylhept-3-en-2-yl]-10,13-dimethyl-2,3,4,9,11,12,14,15,16,17-decahydro-1h-cyclopenta[a]phenanthren-3-ol
14. (3.beta.,22e)-ergosta-5,7,22-trien-3-ol
15. Ergosta-5,7,22-trien-3-ol, (3.beta.,22e)-
16. Ergosta-5,7,22-trien-3-ol
17. Unii-z30ray509f
18. Nsc62791
19. Ccris 7220
20. Hsdb 395
21. Provitamine D2
22. 5,7,22-ergostatrien-3beta-ol
23. Ergosta-5,7,22-trien-3-ol, (3beta,22e)-
24. (3s,9s,10r,13r,14r,17r)-10,13-dimethyl-17-[(e,1r,4r)-1,4,5-trimethylhex-2-enyl]-2,3,4,9,11,12,14,15,16,17-decahydro-1h-cyclopenta[a]phenanthren-3-ol
25. Einecs 200-352-7
26. 3beta-hydroxy-5,7,22-ergostatriene
27. 24alpha-methyl-22e-dehydrocholesterol
28. Ergosterol, >=75%
29. Ergosterol [mi]
30. Ai3-18876
31. Ergosterol [hsdb]
32. Ergosterol [inci]
33. 24r-methylcholesta-5,7,2e-trien-3beta-ol
34. Bmse000494
35. Ergosterol (provitamin D2)
36. Ergosterol [usp-rs]
37. Schembl43194
38. Megxm0_000450
39. Chembl1232562
40. Acon0_000429
41. Acon1_000637
42. Dtxsid90878679
43. 24a-methyl-22e-dehydrocholesterol
44. Ergosterol, >=95.0% (hplc)
45. Hy-n0181
46. Zinc4084618
47. Bdbm50378884
48. Lmst01030093
49. S2297
50. 24alpha-methyl-22e-dehydrocholestero
51. Akos015918128
52. Ac-8370
53. Db04038
54. Ds-4956
55. (24r)-ergosta-5,7,22-trien-3b-ol
56. (3beta)-ergosta-5,7,22-trien-3-ol
57. Ncgc00168889-01
58. Ncgc00168889-02
59. 14-((2e)(1r,4r)-1,4,5-trimethylhex-2-enyl)(1s,5s,2r,11r,14r,15r)-2,15-dimethyl Tetracyclo[8.7.0.0<2,7>.0<11,15>]heptadeca-7,9-dien-5-ol
60. 24-methylcholesta-5,7,22-trien-3b-ol
61. 24r-methylcholesta-5,7,22e-trien-3b-ol
62. (3beta,2e)-ergosta-5,7,22-trien-3-ol
63. Cs-0007890
64. N2279
65. (3beta,22e)-ergosta-5,7,22-trien-3-ol
66. 24r-methylcholesta-5,7,22e-trien-3beta-ol
67. C01694
68. Ergocalciferol Impurity B [ep Impurity]
69. Ergosta-5,7,22-trien-3-ol,(3
70. A,22e)-
71. 003e623
72. Mixed With Plinia Cauliflora Ethyl Acetate Fraction
73. Q143263
74. 45ed0a4c-6fda-443f-b886-d6c805a76af2
75. Ergosterol, 10 Mg/ml In Chloroform, Analytical Standard
76. (3beta,14beta,17alpha,22e)-ergosta-5,7,22-trien-3-ol
77. Ergosterol, European Pharmacopoeia (ep) Reference Standard
78. Ergosterol, United States Pharmacopeia (usp) Reference Standard
79. Mixed With Active Tannen Enriched Fraction Of Plinia Cauliflora
80. Ergosterol (constituent Of Ganoderma Lucidum Fruiting Body) [dsc]
81. Ergosterol, Pharmaceutical Secondary Standard; Certified Reference Material
| Molecular Weight | 396.6 g/mol |
|---|---|
| Molecular Formula | C28H44O |
| XLogP3 | 7.4 |
| Hydrogen Bond Donor Count | 1 |
| Hydrogen Bond Acceptor Count | 1 |
| Rotatable Bond Count | 4 |
| Exact Mass | 396.339216023 g/mol |
| Monoisotopic Mass | 396.339216023 g/mol |
| Topological Polar Surface Area | 20.2 Ų |
| Heavy Atom Count | 29 |
| Formal Charge | 0 |
| Complexity | 712 |
| Isotope Atom Count | 0 |
| Defined Atom Stereocenter Count | 8 |
| Undefined Atom Stereocenter Count | 0 |
| Defined Bond Stereocenter Count | 1 |
| Undefined Bond Stereocenter Count | 0 |
| Covalently Bonded Unit Count | 1 |
Very high levels of vitamin D have been used to treat maternal hypoparathyroidism during pregnancy. In two studies, 15 mothers were treated with doses averaging 107,000 IU/day throughout their pregnancies to maintain maternal calcium levels within the normal range. All of the 27 children were normal at birth & during follow up examinations, ranging up to 16 years. /Vitamin D/
Briggs, G.G, R.K. Freeman, S.J. Yaffe. A Reference Guide to Fetal and Neonatal Risk. Drugs in Pregnancy and Lactation. 4th ed. Baltimore, MD: Williams & Wilkins 1994., p. 899
... Irradiated ergosterol from yeast became the major vitamin D source for food fortification and the treatment of rickets, leading to a public health campaign to eradicate rickets by the 1930s. /Irradiated ergosterol/
Rajakumar K et al; Am J Pub Hlth 97 (10): 1746-54
Vitamin D is excreted into breast milk in limited amounts. A direct relationship exists between maternal serum levels of vitamin D & the concn in breast milk. Chronic maternal ingestion of large doses may lead to greater than normal vitamin D activity in the milk & resulting hypercalcemia in the infant. /Vitamin D/
Briggs, G.G, R.K. Freeman, S.J. Yaffe. A Reference Guide to Fetal and Neonatal Risk. Drugs in Pregnancy and Lactation. 4th ed. Baltimore, MD: Williams & Wilkins 1994., p. 900
Provitamins
Precursor forms of vitamins. (See all compounds classified as Provitamins.)
Vitamin D is excreted into breast milk in limited amounts. A direct relationship exists between maternal serum levels of vitamin D & the concn in breast milk. Chronic maternal ingestion of large doses may lead to greater than normal vitamin D activity in the milk & resulting hypercalcemia in the infant. /Vitamin D/
Briggs, G.G, R.K. Freeman, S.J. Yaffe. A Reference Guide to Fetal and Neonatal Risk. Drugs in Pregnancy and Lactation. 4th ed. Baltimore, MD: Williams & Wilkins 1994., p. 900
The results of experiments on rats given the ergosterol-containing diet for a long time indicate that ergosterol was incorporated in liver tissues in trace amounts which are not comparable with ergosterol concentrations exerting an effect in model experiments. Ergosterol was not detected in the liver after 3-day experiments. At the same time it was established that the proportion of unchanged ergosterol in rat feces was about 16% of the amount administered per os. The products of a possible ergosterol transformation (dehydroneoergosterol-24-methyl-1,3,5 (10), 6,8 (9), 22-hexaen-3 beta-ol; 24-methylcholesta-7,24 (28)-dien-3 beta-ol; 4-cholesta-7,22,25 (?)-trien-3 beta-ol; 4-methylcholesta-7,22 (?)-dien-3 beta-ol, and so forth were identified in feces.
PMID:6523807 Garbuzov AG et al; Voprosy Pitaniia 6: 54-6 (1984)
... The metabolism of ergosterol by cytochrome P450scc /is demonstrated/ in either a reconstituted system or isolated adrenal mitochondria. The major reaction product was identified as 17alpha,24-dihydroxyergosterol. Purified P450scc also generated hydroxyergosterol as a minor product, which is probably an intermediate in the synthesis of 17alpha,24-dihydroxyergosterol. In contrast to cholesterol and 7-dehydrocholesterol, cleavage of the ergosterol side chain was not observed. NMR analysis clearly located one hydroxyl group to C24, with evidence that the second hydroxyl group is at C17. 17alpha,24-Dihydroxyergosterol inhibited cell proliferation of HaCaT keratinocytes and melanoma cells. Thus, in comparison with cholesterol and 7-dehydrocholesterol, the 24-methyl group and the C22-C23 double bond of ergosterol prevent side chain cleavage by P450scc and change the enzyme's hydroxylase activity from C22 and C20, to C24 and C17, generating bioactive product.
PMID:16125105 Slominski A et al; Chem Biol 12 (8): 931-9 (2005)
In order to investigate the effect of the different stereochemistry of C-24 on the microbial C-26 oxidation of sterol side-chain the genetically modified Mycobacterium sp. BCS 396 strain was used to transform erogsterol. Ergosterol was converted to 3-oxo-4,22-ergostadien-26-oic acid methyl ester, 3-oxo-1,4,22-ergostatrien-26-oic acid methyl ester, and 3-oxo-1,4,22-ergostatrien-26-oic acid, the structures of which have been determined by IR, 1H NMR, 13C NMR, and mass spectroscopy. The X-ray structure of 3-oxo-4,22-ergostadien-26-oic acid methyl ester revealed that oxidation at C-26 of the ergostane side-chain generates a chiral center with S-configuration at C-25 as a result of chiral induction of the C-24 center.
PMID:8545852 Ambrus G et al; Steroids 60 (9): 626-9 (1995)
The results of experiments on rats given the ergosterol-containing diet for a long time indicate that ergosterol was incorporated in liver tissues in trace amounts which are not comparable with ergosterol concentrations exerting an effect in model experiments. Ergosterol was not detected in the liver after 3-day experiments. At the same time it was established that the proportion of unchanged ergosterol in rat feces was about 16% of the amount administered per os. The products of a possible ergosterol transformation (dehydroneoergosterol-24-methyl-1,3,5 (10), 6,8 (9), 22-hexaen-3 beta-ol; 24-methylcholesta-7,24 (28)-dien-3 beta-ol; 4-cholesta-7,22,25 (?)-trien-3 beta-ol; 4-methylcholesta-7,22 (?)-dien-3 beta-ol, and so forth were identified in feces.
PMID:6523807 Garbuzov AG et al; Voprosy Pitaniia 6: 54-6 (1984)
Metabolism of orally administered ergosterol (Erg) ... in rats and ... vitamin D biological activity were investigated. Most of orally administered Erg ... /was/ excreted in feces and the remaining sterols were absorbed through intestine. The absorbed sterols were not transported in skin as the intact forms but metabolized into brassicasterol and cholesterol, respectively, within 25 hr. Neither increment of intestinal calcium absorption nor plasma calcium concentrations were observed by oral administration of Erg ... to vitamin D-deficient rats...
PMID:1629783 Tsugawa N et al; J Nutr Sci Vitamology 38 (1): 15-25 (1992)
The chick-oviduct assay was used to investigate the effects of dietary ergosterol on the response to oral progestogens and estrogens. Progestogens alone had no effect on the oviduct but the hypertrophy due to estrogen was greatly enhanced by simultaneous treatment with progestogen at all dose levels tested. Ergosterol had no effect on any of the responses of the oviduct studied.
PMID:71938 Webb GP, Taylor TG; Brit Poul Sci 18 (5): 543-5 (1977)
... A new member of the F-box family, Pof14, which forms a canonical, F-box dependent SCF (Skp1, Cullin, F-box protein) ubiquitin ligase complex /is described/. The Pof14 protein has intrinsic instability that is abolished by inactivation of its Skp1 interaction motif (the F-box), Skp1 or the proteasome, indicating that Pof14 stability is controlled by an autocatalytic mechanism. Pof14 interacts with the squalene synthase Erg9, a key enzyme in ergosterol metabolism, in a membrane-bound complex that does not contain the core SCF components. pof14 transcription is induced by hydrogen peroxide and requires the Pap1 transcription factor and the Sty1 MAP kinase. Pof14 binds to and decreases Erg9 activity in vitro and a pof14 deletion strain quickly loses viability in the presence of hydrogen peroxide due to its inability to repress ergosterol synthesis. A pof14 mutant lacking the F-box and an skp1-3 ts mutant behave as wild type in the presence of oxidant showing that Pof14 function is independent of SCF. This indicates that modulation of ergosterol level plays a key role in adaptation to oxidative stress.
PMID:17016471 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1589992 Tafforeau L et al; EMBO J; 25 (19): 4547-56 (2006)
The continuous use of triazoles can result in the development of drug resistance. Azole-resistant clinical isolates, spontaneous and induced mutants of Aspergillus fumigatus have been documented. The azoles block the ergosterol biosynthesis pathway by inhibiting the enzyme 14-alpha-demethylase, product of the CYP51. Fungal azole resistance involves both amino acid changes in the target site that alter drug-target interactions and those that decrease net azole accumulation. The reduced intracellular accumulation has also been correlated with overexpression of multidrug resistance (MDR) efflux transporter genes of the ATP-binding cassette (ABC) and the major facilitator superfamily (MFS) classes. About 20 genes are involved in the A. fumigatus ergosterol biosynthesis pathway. There are several duplicated genes in this pathway. Interestingly, erg3 and erg11 showed two copies in A. fumigatus. In general, Aspergillus spp. have proportionally more MFS transporter encoding genes than Saccharomyces cerevisiae, S. pombe, and Neurospora crassa. The drug H+ (12 and 14 spanners) sub-families are also proportionally greater than in the other species. Although the numbers of ABC transporter encoding genes are comparable, again the Aspergillus spp. have more ABC transporters related to multidrug permease than the other fungal species.
PMID:16110826 Ferreira ME da Silva et al; 43 (1): 313-9 (2005)
The human pathogen Candida albicans is responsible for a large proportion of infections in immunocompromised individuals, and the emergence of drug-resistant strains is of medical concern. Resistance to antifungal azole compounds is often due to an increase in drug efflux or an alteration of the pathway for synthesis of ergosterol, an important plasma membrane component in fungi. However, little is known about the transcription factors that mediate drug resistance. In Saccharomyces cerevisiae, two highly related transcriptional activators, Upc2p and Ecm22p, positively regulate the expression of genes involved in ergosterol synthesis (ERG genes). ... A homologue in C. albicans of the S. cerevisiae UPC2/ECM22 genes ... named ... UPC2 /has been identified/. Deletion of this gene impaired growth under anaerobic conditions and rendered cells highly susceptible to the antifungal drugs ketoconazole and fluconazole. Conversely, overexpression of Upc2p increased resistance to ketoconazole, fluconazole, and fluphenazine. Azole-induced expression of the ERG genes was abolished in a Delta upc2 strain, while basal levels of these mRNAs remained unchanged. Importantly, the purified DNA binding domain of Upc2p bound in vitro to putative sterol response elements in the ERG2 promoter, suggesting that Upc2p increases the expression of the ERG genes by directly binding to their promoters. These results provide an important link between changes in the ergosterol biosynthetic pathway and azole resistance in this opportunistic fungal species.
PMID:15855491 Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1087678 MacPherson S et al; Antimicrob Agent Chemother 49 (5): 1745-52 (2005)
Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. ... Specific inhibitors /were used/ to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A2 (PLA2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA2, arachidonic acid trifluoromethyl ketone (AACOCF3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and DeltapH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA2 and PKC.
PMID:15191747 Kasparovsky T et al; Plant Physiol Biochem 42 (5): 429-35 (2004)
For more Mechanism of Action (Complete) data for ERGOSTEROL (7 total), please visit the HSDB record page.
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