Glucocorticoid receptor [1,2]

- Effect on embryo development: Hydrocortisone acetate affects the development of mouse embryos. It can cause macroscopic - visible dilatation of the venous marginal blood sinus of the foot plates in mouse embryos. It may also lead to other developmental abnormalities, interfering with normal limb development [1]
- Effect on immunoglobulin metabolism: In normal and low - pathogen mice, Hydrocortisone acetate reduces the serum concentration of all sub - classes of IgG (γ2a, γ2b, and γ1), as well as IgA and IgM. Turnover studies using 131I - labeled γ2a subclass of IgG show that high - dose corticosteroids cause a significantly shortened survival (increased catabolic rate) of IgG, contributing to hypogammaglobulinemia. The increase in fractional catabolism is due to an increase in endogenous catabolism, not excess loss in the urine or stool [2]

- Embryo development experiment: Pregnant mice were injected with Hydrocortisone acetate at a certain dose during pregnancy. The specific injection dose and frequency are not mentioned in the literature. After a certain period, the embryos were isolated, and the morphological changes of the embryos were observed, especially the development of the foot plates, to assess the impact of Hydrocortisone acetate on embryo development [1]
- Immunoglobulin metabolism experiment: Normal and low - pathogen mice were given Hydrocortisone acetate, and the administration route, dose, and frequency are not mentioned in the literature. Blood samples were taken at different time points, and the serum concentrations of IgG sub - classes, IgA, and IgM were measured. 131I - labeled γ2a subclass of IgG was used for turnover studies, and the catabolic rate of IgG was calculated by detecting the radioactivity in the blood [2]
- Additional Info - Hydrocortisone acetate is a corticosteroid drug. Its mechanism of action may be related to binding to the glucocorticoid receptor, regulating gene expression, and then affecting various physiological processes. It has a cell - stabilizing effect, which can stabilize lipoprotein membranes and prevent lysosomes from releasing hydrolytic enzymes. However, in some cases, it may also delay the repair of cellular injury, possibly due to the stimulation of the synthesis of enzymes deaminating amino acids [1]

Absorption, Distribution and Excretion
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.

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Metabolism / Metabolites
Primarily hepatic via CYP3A4

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Biological Half-Life
6-8 hours

Protein Binding
95%

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5744 rat LDLo subcutaneous 250 mg/kg Arzneimittel-Forschung. Drug Research., 27(2102), 1977 [PMID:580008]
5744 mouse LD50 intraperitoneal 2300 mg/kg Compilation of LD50 Values of New Drugs.
5744 mouse LD50 subcutaneous 45050 ug/kg National Cancer Institute Screening Program Data Summary, Developmental Therapeutics Program., JAN1986

[1]. The effect of hydrocortisone acetate on the development of mouse embryos. J Embryol Exp Morphol. 1968 Nov;20(3):355-66.
[2]. The effect of hydrocortisone on immunoglobulin metabolism. J Clin Invest. 1970 Sep;49(9):1679-84.

Cortisol 21-acetate is a tertiary alpha-hydroxy ketone and a cortisol ester.
Hydrocortisone Acetate is the synthetic acetate ester form of hydrocortisone, a corticosteroid with anti-inflammatory and immunosuppressive properties. Hydrocortisone acetate initially binds to the cytoplasmic glucocorticoid receptor; then the receptor-ligand complex is translocated to the nucleus where it initiates the transcription of genes encoding for anti-inflammatory mediators, such as cytokines and lipocortins. Lipocortins inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and preventing the synthesis of prostaglandins and leukotrienes.
See also: Hydrocortisone Acetate; Pramoxine Hydrochloride (component of); Hydrocortisone Acetate; Neomycin Sulfate (component of); Chloramphenicol; hydrocortisone acetate (component of) ... View More ...

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Drug Indication
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.

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Mechanism of Action
Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

C23H32O6

404.4966

404.219

C, 68.29; H, 7.97; O, 23.73

50-03-3

Hydrocortisone 17-butyrate;13609-67-1;Hydrocortisone 17-valerate;57524-89-7;Hydrocortisone hemisuccinate;2203-97-6;Hydrocortisone;50-23-7;Hydrocortisone phosphate;3863-59-0

5744

White to light yellow solid powder

1.3±0.1 g/cm3

576.6±50.0 °C at 760 mmHg

223 °C (dec.)(lit.)

196.2±23.6 °C

0.0±3.6 mmHg at 25°C

1.573

2.51

2

6

4

29

786

7

CC(=O)OCC(=O)[C@]1(CC[C@@H]2[C@@]1(C[C@@H]([C@H]3[C@H]2CCC4=CC(=O)CC[C@]34C)O)C)O

ALEXXDVDDISNDU-JZYPGELDSA-N

InChI=1S/C23H32O6/c1-13(24)29-12-19(27)23(28)9-7-17-16-5-4-14-10-15(25)6-8-21(14,2)20(16)18(26)11-22(17,23)3/h10,16-18,20,26,28H,4-9,11-12H2,1-3H3/t16-,17-,18-,20+,21-,22-,23-/m0/s1

[2-[(8S,9S,10R,11S,13S,14S,17R)-11,17-dihydroxy-10,13-dimethyl-3-oxo-2,6,7,8,9,11,12,14,15,16-decahydro-1H-cyclopenta[a]phenanthren-17-yl]-2-oxoethyl] acetate

hydrocortisone acetate; 50-03-3; Cortisol 21-acetate; Hydrocortisone 21-acetate; Cortell; Cortifoam; Cortef acetate; Cortisol acetate;

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 : ≥ 38 mg/mL (~93.94 mM)
H2O : ~1 mg/mL (~2.47 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.18 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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