| Size | Price | Stock | Qty |
|---|---|---|---|
| 250mg |
|
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| Other Sizes |
| Targets |
Mineralocorticoid receptor (agonist) [4]
|
|---|---|
| ln Vivo |
In uninephrectomized rats, subcutaneous administration of Deoxycorticosterone Acetate (15 mg/kg) twice weekly, combined with 1% NaCl in drinking water, induced a progressive and significant increase in systolic blood pressure over a 4-week period. Two weeks of treatment caused mild hypertension, and by 4 weeks, systolic blood pressure reached 185 ± 6 mmHg compared to 118 ± 3 mmHg in uninephrectomized control rats. [4]
Deoxycorticosterone Acetate-salt treatment resulted in significantly increased heart weight/body weight ratio, left ventricular weight/body weight ratio, and left kidney weight/body weight ratio at 4 weeks, indicating cardiac and renal hypertrophy. [4] Deoxycorticosterone Acetate-salt treatment led to significant renal dysfunction at 4 weeks, characterized by increased urinary protein excretion, decreased creatinine clearance, elevated fractional excretion of sodium (FENa), increased urinary N-acetyl-β-glucosaminidase (NAG) activity, and decreased renal blood flow. [4] Histological examination revealed that Deoxycorticosterone Acetate-salt treatment caused renal damage including tubular dilatation and atrophy, as well as thickening of small arteries. It also induced vascular hypertrophy in the aorta, evidenced by significant increases in wall thickness, wall area, and wall-to-lumen ratio. [4] Deoxycorticosterone Acetate-salt treatment also resulted in reduced body weight gain compared to control animals over the 4-week study period. [4] |
| Animal Protocol |
Induction of DOCA-Salt Hypertension:** Male Sprague-Dawley rats (160-180 g) underwent right uninephrectomy under pentobarbital anesthesia. After a one-week recovery, hypertension was induced by subcutaneous administration of Deoxycorticosterone Acetate (15 mg/kg) suspended in corn oil, twice weekly. Concurrently, animals were provided with 1% NaCl solution as drinking water ad libitum. Control animals were uninephrectomized but did not receive Deoxycorticosterone Acetate or salt. The treatment continued for 4 weeks. Systolic blood pressure was monitored weekly via the tail-cuff method. [4]
* **Sample and Tissue Collection:** At the end of the 4-week experimental period, urine was collected overnight using metabolic cages. Animals were then anesthetized for renal blood flow measurement. After exsanguination, blood samples were collected, and the heart, left kidney, and aorta were excised for weight measurements and histological analysis. [4] Induction of DOCA-Salt Hypertension: Male Sprague-Dawley rats (160-180 g) underwent right uninephrectomy under pentobarbital anesthesia. After a one-week recovery, hypertension was induced by subcutaneous administration of Deoxycorticosterone Acetate (15 mg/kg) suspended in corn oil, twice weekly. Concurrently, animals were provided with 1% NaCl solution as drinking water ad libitum. Control animals were uninephrectomized but did not receive Deoxycorticosterone Acetate or salt. The treatment continued for 4 weeks. Systolic blood pressure was monitored weekly via the tail-cuff method. [4] Sample and Tissue Collection: At the end of the 4-week experimental period, urine was collected overnight using metabolic cages. Animals were then anesthetized for renal blood flow measurement. After exsanguination, blood samples were collected, and the heart, left kidney, and aorta were excised for weight measurements and histological analysis. [4] |
| Toxicity/Toxicokinetics |
The compound is used experimentally to induce a well-characterized model of hypertension, which is associated with significant cardiovascular and renal pathology. [4]
|
| References |
|
| Additional Infomation |
Deoxycorticosterone acetate is a corticosteroid hormone. It is a 21-acetic acid derivative of deoxycorticosterone. See also: Deoxycorticosterone (with active moiety).
Deoxycorticosterone Acetate is a mineralocorticoid hormone. In experimental research, it is used in combination with a high-salt diet and uninephrectomy to induce a robust model of salt-sensitive hypertension in rats. This model is characterized by elevated blood pressure, cardiovascular hypertrophy, and progressive renal injury, and is associated with activation of the endothelin system. [4] The DOCA-salt model is widely used to study the pathophysiology of hypertension and to evaluate the efficacy of potential antihypertensive and organ-protective agents. This study specifically utilized the model to investigate the differential roles of endothelin A and B receptors in hypertension and end-organ damage. [4] |
| Exact Mass |
372.23
|
|---|---|
| CAS # |
56-47-3
|
| Related CAS # |
Deoxycorticosterone acetate;56-47-3
|
| PubChem CID |
5952
|
| Appearance |
White to off-white solid powder
|
| Density |
1.1±0.1 g/cm3
|
| Boiling Point |
504.1±50.0 °C at 760 mmHg
|
| Melting Point |
157°C
|
| Flash Point |
218.0±30.2 °C
|
| Vapour Pressure |
0.0±1.3 mmHg at 25°C
|
| Index of Refraction |
1.542
|
| Source |
Endogenously produced metabolite
|
| LogP |
4.53
|
| Hydrogen Bond Donor Count |
0
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
4
|
| Heavy Atom Count |
27
|
| Complexity |
707
|
| Defined Atom Stereocenter Count |
6
|
| SMILES |
O=C(C([H])([H])OC(C([H])([H])[H])=O)[C@@]1([H])C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])C4=C([H])C(C([H])([H])C([H])([H])[C@]4(C([H])([H])[H])[C@@]3([H])C([H])([H])C([H])([H])[C@@]21C([H])([H])[H])=O
|
| InChi Key |
VPGRYOFKCNULNK-ACXQXYJUSA-N
|
| InChi Code |
InChI=1S/C23H32O4/c1-14(24)27-13-21(26)20-7-6-18-17-5-4-15-12-16(25)8-10-22(15,2)19(17)9-11-23(18,20)3/h12,17-20H,4-11,13H2,1-3H3/t17-,18-,19-,20+,22-,23-/m0/s1
|
| Chemical Name |
[2-[(8S,9S,10R,13S,14S,17S)-10,13-dimethyl-3-oxo-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-17-yl]-2-oxoethyl] acetate
|
| Synonyms |
DOCA PercotolDeoxycorticosterone Acetate Cortexone acetate
|
| HS Tariff Code |
2934.99.9001
|
| 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)
|
| Solubility (In Vitro) |
DMSO : ~41.67 mg/mL (~111.87 mM)
H2O : ~1 mg/mL (~2.68 mM) |
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.08 mg/mL (5.58 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (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 DMSO stock solution (20.8 mg/mL) to 900 μL of 20% SBE-β-CD saline and mix well. 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. Solubility in Formulation 2: ≥ 2.08 mg/mL (5.58 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 DMSO stock solution (20.8 mg/mL) to 900 μL of corn oil and mix well. Solubility in Formulation 3: ≥ 1.67 mg/mL (4.48 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (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 DMSO stock solution (16.7 mg/mL) to 400 μL of PEG300 and mix well; then add 50 μL of Tween-80 and mix well; finally add 450 μL of physiological saline and adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. (Please use freshly prepared in vivo formulations for optimal results.) |
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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT01186484 | COMPLETED | Drug: JNJ-212082 | Prostatic Neoplasms | Janssen Pharmaceutical K.K. | 2010-06-01 | Phase 1 |
| NCT00473512 | COMPLETEDWITH RESULTS | Drug: Abiraterone acetate Drug: Abiraterone acetate MTD Drug: Dexamethasone |
Prostatic Neoplasms | Cougar Biotechnology, Inc. | 2005-11 | Phase 1 Phase 2 |
| NCT03082339 | COMPLETED | Other: Cortisone | QTc-interval | Asklepios Neurological Clinic Bad Salzhausen | 2017-04-01 |
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