Ergosterol is a sterol that was isolated from Grifola frondosa that has applications in the research of allergy disorders that depend on mast cells. Ergosterol (10, 20, and 50 μM) suppresses the release of histamine and beta-hexosaminidase in response to antigen stimulation in RBL-2H3 cells. The levels of TNF-α and IL-4 mRNA were dramatically decreased by ergosterol (20 and 50 μM). FcεRI aggregation generated by antigen is inhibited by ergosterol (50 μM) [1].

Ergosterol (25, 50 mg/kg, oral) enhanced SOD activity, decreased the production of MDA, CK-MB, and LDH in LPS-induced septic rats, and considerably mitigated the LPS-induced decline in cardiac function in rats [2].

Absorption, Distribution and Excretion
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/
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.

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Metabolism / Metabolites
... 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.
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.
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.
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...
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.

Interactions
MURINE LEUKEMIA CELLS (L1210) GROWN IN MEDIUM CONTAINING ERGOSTEROL (40 UG/ML) THEN EXPOSED BRIEFLY TO AMPHOTERICIN B (0-10 UG/ML) WERE MORE SENSITIVE TO THE ANTIBIOTIC THAN WERE CONTROLS.
AFTER 4-HR GROWTH PERIOD IN PRESENCE OF 5X10-9 MOLES KETOCONAZOLE, ACETATE INCORPORATION INTO ERGOSTEROL BY CANDIDA ALBICANS WAS INHIBITED APPROXIMATELY 50%.
INHIBITION OF ERGOSTEROL BIOSYNTHESIS IN CANDIDA ALBICANS BY THE ANTIFUNGAL AGENT MICONAZOLE NITRATE WAS INVESTIGATED AFTER IN VITRO CONTACT WITH THE DRUG FOR 1, 4, 16, & 24 HR.
The functions and biosynthesis of sterols have been effective targets for fungal control in different areas, including pharmaceutical and agricultural applications. Fungi are among the organisms that synthesize sterols, principally ergosterol. In this paper, the effect of dibutyryl-cAMP (db-cAMP) on ergosterol level and the interaction of drugs that would change the concentration of cAMP with antifungal drugs have been investigated. Sterols were extracted from Candida albicans, and ergosterol was measured using the gas chromatography method. The interaction of different agents was measured by the broth dilution method. It was found that phosphodiesterase inhibitors reverse the inhibitory activity of azole antifungal drugs. Evaluating the ergosterol level of C. albicans incubated with db-cAMP revealed that it increased ergosterol level. Further experiments provided evidence attributing the observed interaction between azoles and phosphodiesterase inhibitors to the relationship between ergosterol and cAMP. The possible significance of this interaction includes potentiation of antifungal activity of drugs by manipulating the cAMP level.
For more Interactions (Complete) data for ERGOSTEROL (6 total), please visit the HSDB record page.

[1]. Kawai J, et al. Ergosterol and its derivatives from Grifola frondosa inhibit antigen-induced degranulation of RBL-2H3 cells by suppressing the aggregation of high affinity IgE receptors. Biosci Biotechnol Biochem. 2018 Jul 2:1-9.
[2]. Xu J, et al. Ergosterol Attenuates LPS-Induced Myocardial Injury by Modulating Oxidative Stress and Apoptosis in Rats. Cell Physiol Biochem. 2018;48(2):583-592

Therapeutic Uses
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/
... 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/

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Drug Warnings
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/

C28H44O

396.65

396.339

57-87-4

444679

White to yellow solid powder

1.0±0.1 g/cm3

501.5±39.0 °C at 760 mmHg

156-158 °C(lit.)

216.3±19.3 °C

0.0±2.9 mmHg at 25°C

1.543

9.3

1

1

4

29

712

8

C[C@H](/C=C/[C@H](C)C(C)C)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3C2=CC=C4[C@@]3(CC[C@@H](C4)O)C)C

DNVPQKQSNYMLRS-APGDWVJJSA-N

InChI=1S/C28H44O/c1-18(2)19(3)7-8-20(4)24-11-12-25-23-10-9-21-17-22(29)13-15-27(21,5)26(23)14-16-28(24,25)6/h7-10,18-20,22,24-26,29H,11-17H2,1-6H3/b8-7+/t19-,20+,22-,24+,25-,26-,27-,28+/m0/s1

(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

Provitamin D2; Provitamin D; Ergosterol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~3.57 mg/mL (~9.00 mM)
Ethanol : ~2.6 mg/mL (~6.55 mM)

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)