| Size | Price | Stock | Qty |
|---|---|---|---|
| 100mg |
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| 500mg |
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| Targets |
Glucocorticoid receptor (GR)
The primary target of this drug is the glucocorticoid receptor (GR). After administration, its active form, hydrocortisone, binds with high affinity to the cytosolic glucocorticoid receptor. The activated receptor-ligand complex translocates to the nucleus, where it acts as a transcription factor to regulate the expression of downstream target genes, forming the molecular basis for its anti-inflammatory and immunosuppressive effects. |
|---|---|
| ln Vitro |
Suppressed IL-6-dependent proliferation of MH60.BSF2 cells (IC₅₀ = 3.5 × 10⁻⁷ M)[1]
Inhibited lymphocyte proliferation in human tonsil cell cultures (91% inhibition at 10⁻⁵ M)[3] Hydrocortisone sodium succinate exhibits significant immunosuppressive activity in vitro. Data show that it effectively inhibits IL-6 bioactivity with an IC50 of approximately 6.7 μM. Additionally, it inhibits IL-3 activity (IC50 of 21.4 μM). At the cellular level, treatment with this compound (0.12 – 60 μM) for 72 hours significantly suppresses phytohemagglutinin (PHA)-stimulated proliferation in human T lymphocytes and peripheral lymphocytes, achieving up to 91% inhibition of human tonsil cell proliferation at 10⁻⁵ M. With an IC50 of 6.7 and 21.4 μM, respectively, hydrocortisone sodium hemisuccinate suppresses the biological activities of IL-6 and IL-3. It has no cytotoxic effect on MH60 cells that are IL-6-independent [3]. In T lymphocyte and peripheral lymphocyte cultures, hydrocortisone sodium hemisuccinate (0.12–60 μM; 72 hours) suppresses phytohemagglutinin (PHA) responses [3]. |
| ln Vivo |
Loaded in pH-sensitive hydrogel significantly reduced colitis symptoms in mice (DAI score 1.8 vs. 4.2 in control)[2]
In mice, oral administration of hydrocortisone sodium hemisuccinate (30 mg/kg) twice a day for five days results in decreased weight loss and increased food intake [2]. In animal models, Hydrocortisone sodium succinate demonstrates clear anti-inflammatory and colitis treatment effects. In a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced mouse model of ulcerative colitis, oral or rectal administration significantly reduces the disease activity index (DAI) and myeloperoxidase (MPO) activity, while alleviating colon shortening. In one study, a pH-sensitive hydrogel loaded with this drug (15% w/w drug content) effectively ameliorated colitis symptoms in a rat model, showing superior effects compared to the standard drug control group. |
| Enzyme Assay |
Although detailed non-cellular protocols for this specific compound are limited, classic glucocorticoid receptor binding assays typically employ a radioligand binding method. The brief protocol is as follows: Prepare a cytosol fraction rich in glucocorticoid receptors (typically from rat liver or thymus) and incubate it with serial concentrations of Hydrocortisone sodium succinate and a fixed concentration of a radiolabeled ligand (e.g., ³H-dexamethasone) at 4°C overnight. After incubation, separate bound and free ligands using dextran-coated charcoal (DCC) and measure radioactivity with a scintillation counter. Calculate the IC50 (concentration required to inhibit 50% of radioligand binding) or Ki from the competition curve.
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| Cell Assay |
IL-6 bioactivity assay: MH60.BSF2 cells cultured with IL-6 and test compounds for 44h. Cell viability measured via MTT assay. Hydrocortisone hemisuccinate dissolved in ethanol and diluted in medium[1]
Lymphocyte suppression: Human tonsil cells cultured with phytohemagglutinin for 72h. Hydrocortisone hemisuccinate added at initiation. Proliferation assessed via ³H-thymidine incorporation[3] The IL-6-dependent MH60.BSF2 cell line is commonly used to evaluate the inhibitory activity of this compound. A standard protocol is as follows: Seed MH60.BSF2 cells (in log phase) into a 96-well plate. Add a fixed concentration of recombinant IL-6 and serially diluted Hydrocortisone sodium succinate (typically dissolved in DMSO or ethanol and then diluted with medium) to the wells. After incubation for 44 hours at 37°C in a 5% CO₂ incubator, add MTT reagent (final concentration 0.5 mg/mL) and incubate for an additional 4 hours. Finally, add a lysis solution (e.g., DMSO or acidified isopropanol) to dissolve the formazan crystals and measure absorbance at 570 nm. Evaluate in vitro activity by calculating the IC50 for inhibition of IL-6-dependent cell proliferation. |
| Animal Protocol |
Colitis treatment: Hydrocortisone hemisuccinate loaded in hydrogel (drug content 15% w/w). Administered rectally (100 mg/kg) to DSS-induced colitis mice daily for 7 days[2]
Animal/Disease Models: Male SD (SD (Sprague-Dawley)) rats (200-220 g, 10-11 weeks) induced colitis [2] Doses: 30 mg/kg Route of Administration: Po twice (two times) daily for 5 days Experimental Results: Significant reduction in disease Activity index (DAI) scores and myeloperoxidase (MPO) activity compared with the 2,4,6-trinitrobenzene sulfonic acid (TNBS) group. Weight gain. The most representative method is the use of a TNBS-induced ulcerative colitis (UC) mouse model for pharmacodynamic evaluation. The procedure is as follows: After fasting for 24 hours, male SD rats or mice are intrarectally infused with a 50% ethanol solution containing 2.5% TNBS to induce colitis. After modeling, animals are randomly divided into model, positive control, and treatment groups. Animals in the treatment group receive Hydrocortisone sodium succinate, e.g., at a dose of 30 mg/kg orally twice daily for 5 days. At the experimental endpoint, samples are collected after the final dose. Evaluation metrics include body weight change, disease activity index (DAI) score, colon length measurement, myeloperoxidase (MPO) activity in colon tissue, and organ indices (e.g., spleen and thymus). |
| ADME/Pharmacokinetics |
The colon-targeting hydrogel showed a drug release rate of less than 10% at pH 1.2 (stomach) and more than 80% at pH 7.4 (colon) [2]
As a water-soluble prodrug, Hydrocortisone sodium succinate is rapidly absorbed and activated. After IV or IM administration, it is quickly hydrolyzed to its active form, hydrocortisone. Its biological half-life is approximately 100 minutes (1.5-2 hours), but its duration of biologic action is longer (approximately 1.25-1.5 days) due to its genomic effects. Plasma protein binding is high (>90%), primarily to corticosteroid-binding globulin and albumin. The drug is mainly metabolized in the liver to metabolites like tetrahydrocortisone and glucuronide conjugates, with only a trace amount excreted unchanged in the urine. |
| Toxicity/Toxicokinetics |
Compared with mucosal atrophy induced by free drugs, no obvious histological damage was observed in the colonic tissue [2]
The toxicity of Hydrocortisone sodium succinate is closely related to dosage and duration of therapy. Long-term, high-dose use can lead to a range of serious adverse reactions, including iatrogenic hyperadrenocorticism (Cushing's syndrome, characterized by moon face, central obesity, hypertension, hyperglycemia), increased risk of infection (due to immunosuppression), peptic ulcers with potential perforation and hemorrhage, osteoporosis, muscle wasting, and psychiatric disturbances (euphoria, insomnia, depression). Prolonged use in children can inhibit growth and development. Rapid intravenous administration of high doses may cause immediate hypersensitivity reactions. Gradual tapering is essential upon discontinuation to avoid iatrogenic adrenal insufficiency. |
| References |
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| Additional Infomation |
Hydrocortisone succinate is a derivative of succinic acid, in which one of its carboxyl groups is esterified with the C-21 hydroxyl group of cortisol (hydrocortisone). It is a dicarboxylic acid monoester, hemisuccinate, and tertiary α-hydroxy ketone. Its function is related to cortisol. Hydrocortisone sodium succinate is the sodium salt of hydrocortisone succinate and possesses glucocorticoid properties. The chemical structure of hydrocortisone sodium succinate is similar to that of endogenous hormones, stimulating anti-inflammatory and immunosuppressive activity, and exhibiting mild mineralocorticoid activity. The drug binds to intracellular glucocorticoid receptors and translocates to the cell nucleus, where it initiates the transcription of glucocorticoid-responsive genes (such as various cytokines and lipocortin). Lipocortin inhibits phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and inhibiting the synthesis of prostaglandins and leukotrienes, both potent inflammatory mediators. Hydrocortisone hemisuccinate is the synthetic hemisuccinate form of hydrocortisone, a corticosteroid with anti-inflammatory and immunosuppressive effects. Hydrocortisone acetate first binds to cytoplasmic glucocorticoid receptors; then, the receptor-ligand complex translocates to the cell nucleus, where it initiates the transcription of genes encoding anti-inflammatory mediators such as cytokines and lipocortin. Lipocorticoids inhibit phospholipase A2, thereby blocking the release of arachidonic acid from membrane phospholipids and inhibiting the synthesis of prostaglandins and leukotrienes.
|
| Molecular Formula |
C25H33NAO8
|
|---|---|
| Molecular Weight |
484.52
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| Exact Mass |
484.207
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| Elemental Analysis |
C, 61.97; H, 6.87; Na, 4.74; O, 26.42
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| CAS # |
125-04-2
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| Related CAS # |
Hydrocortisone hemisuccinate;2203-97-6
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| PubChem CID |
16623
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| Appearance |
White to off-white solid powder
|
| Boiling Point |
685.5ºC at 760mmHg
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| Flash Point |
231.1ºC
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| Vapour Pressure |
9.36E-22mmHg at 25°C
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| LogP |
0.862
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| Hydrogen Bond Donor Count |
3
|
| Hydrogen Bond Acceptor Count |
8
|
| Rotatable Bond Count |
7
|
| Heavy Atom Count |
33
|
| Complexity |
908
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| Defined Atom Stereocenter Count |
7
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| SMILES |
C[C@]12CCC(=O)C=C1CC[C@@H]3[C@@H]2[C@H](C[C@]4([C@H]3CC[C@@]4(C(=O)COC(=O)CCC(=O)O)O)C)O
|
| InChi Key |
VWQWXZAWFPZJDA-CGVGKPPMSA-N
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| InChi Code |
InChI=1S/C25H34O8/c1-23-9-7-15(26)11-14(23)3-4-16-17-8-10-25(32,24(17,2)12-18(27)22(16)23)19(28)13-33-21(31)6-5-20(29)30/h11,16-18,22,27,32H,3-10,12-13H2,1-2H3,(H,29,30)/t16-,17-,18-,22+,23-,24-,25-/m0/s1
|
| Chemical Name |
4-[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-oxoethoxy]-4-oxobutanoic acid
|
| Synonyms |
Hydrocortisone sodium succinate; 125-04-2; A-hydroCort; Solu-Cortef; Nositrol; Cortop; Cortisol 21-(sodium succinate); Flebocortid;
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples
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|---|---|
| Solubility (In Vivo) |
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.
Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.0639 mL | 10.3195 mL | 20.6390 mL | |
| 5 mM | 0.4128 mL | 2.0639 mL | 4.1278 mL | |
| 10 mM | 0.2064 mL | 1.0319 mL | 2.0639 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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