Glucocorticoid receptor [1,2]

- 对胚胎发育的影响：醋酸氢化可的松会影响小鼠胚胎的发育，可导致小鼠胚胎足板的边缘静脉血窦出现肉眼可见的扩张，还可能引发其他发育异常，干扰肢体的正常发育 [1]
- 对免疫球蛋白代谢的影响：在正常和低病原体小鼠中，醋酸氢化可的松可降低IgG所有亚类（γ2a、γ2b和γ1）以及IgA和IgM的血清浓度。使用131I标记的IgG γ2a亚类进行的周转研究表明，高剂量的皮质类固醇会导致IgG的存活时间显著缩短（分解代谢速率增加），从而导致低丙种球蛋白血症。分解代谢分数的增加是由于内源性分解代谢增加，而不是尿液或粪便中的过量流失 [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.

---

Metabolism / Metabolites
Primarily hepatic via CYP3A4

---

Biological Half-Life
6-8 hours

Protein Binding
95%

---

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 ...

---

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.

---

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

100.9

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

注意： 本产品在运输和储存过程中需避光。

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)

配方 1 中的溶解度: ≥ 2.5 mg/mL (6.18 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

---

请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。