17Alpha-hydroxyprogesterone - CAS 68-96-2
Catalog number: 68-96-2
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
17α-Hydroxy Progesterone, as a metabolite of Progesterone, is an endogenous progestogen as well as chemical intermediate in the biosynthesis of other steroid hormones
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Hydroxyprogesterone; (8R,9S,10R,13S,14S,17R)-17-acetyl-17-hydroxy-10,13-dimethyl-2,6,7,8,9,11,12,14,15,16-decahydro-1H-cyclopenta[a]phenanthren-3-one;
Soluble in DMSO
Store at -20 °C
Progesteron. It was isolated from adrenal glands.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
217-221 °C
1.15 g/cm3
Canonical SMILES:
1.Prevention of preterm delivery with compounded 17a-hydroxyprogesterone caproate.
Reed-Kane D Pharmd Fiacp Faca Fc1, Kirschbaum K Phd. Int J Pharm Compd. 2006 May-Jun;10(3):165-71.
17a-hydroxyprogesterone caproate is a naturally occurring metabolite of progesterone that is produced in significant quantities during pregnancy. The demand for 17a-hydroxyprogesterone caproate, the lack of a commercially available manufactured form approved by the US Food And Drug Administration, and publication of the results of a large trial to determine the effectivenss of the drug in the prevention of preterm delivery have spawned an increased interest in compounded formulations of the drug. The demand also has necessitated a review of the available literature and of past clinical studies, and a look at present and planned studies. Owing to the importance of this drug in pregnancy and the need for safety, accuracy in potency, and sterility in an intramuscular injection (the most common route of administration), compounding pharmacies must be in compliance with the United States Pharmacopeia Chapter 797 standards should they wish to compound this formulation.
2.Low basal androstenedione levels plus augmented 17alpha-hydroxyprogesterone and low dehydroepiandrosterone sulfate responses to adrenocorticotropic hormone stimulation in patients with adrenal incidentaloma.
Ozgen AG1, Bayraktar F, Yilmaz C. Endocr Pract. 2001 Nov-Dec;7(6):448-53.
OBJECTIVE: To investigate the androstenedione, 17a-hydroxyprogesterone (17-OHP), and dehydroepiandrosterone sulfate (DHEAS) basal levels and responses to adrenocorticotropic hormone (ACTH) in patients with adrenal incidentalomas in order to determine which enzyme defects are present.
3.Congenital adrenal hyperplasia due to 21-hydroxylase deficiency - management in adults.
Ambroziak U, Bednarczuk T, Ginalska-Malinowska M, Małunowicz EM, Grzechocińska B, Kamiński P, Bablok L, Przedlacki J, Bar-Andziak E. Endokrynol Pol. 2010 Jan-Feb;61(1):142-55.
Congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency is one of the most common autosomal recessive hereditary diseases. The impairment of cortisol synthesis leads to excessive stimulation of the adrenal glands by adrenocorticotropic hormone (ACTH), adrenal hyperplasia, and excessive androgen synthesis. The syndrome is characterised by a considerable correlation between the genotype and the phenotype with the type of CYP21A2 gene mutation affecting the severity of 21-hydroxylase deficiency. The clinical manifestations of CAH in adults result from adrenocortical and adrenomedullary insufficiency, hyperandrogenism, and the adverse effects of glucocorticosteroids used for the treatment of the condition. Non-classic CAH may sometimes be asymptomatic. In patients with classic CAH obesity, hyperinsulinaemia, insulin resistance, and hyperleptinaemia are more often seen than in the general population. These abnormalities promote the development of metabolic syndrome and its sequelae, including endothelial dysfunction, and cardiovascular disease.
4.In vitro-metabolism of 3H-progesterone in human testicular tissue: IV Before and after long-term gonadotrophin treatment; including one 47, XYY-male.
Berg AA, Kjessler B. Acta Endocrinol Suppl (Copenh). 1976;207:49-59.
Certain defects in the intratesticular androgen biogenetic system may lead to a significant impairment of gonadal function in total in the human male. In the present investigation, four males with impaired reproductive performance were analysed before and after long term treatment with gonadotrophic hormones with regard to their in vitro metabolism of 3H-progesterone in testicular incubates; one of whom representing the first instance of an XYY-male studied in some detail with regard to intratesticular steroidogenesis. A steroid metabolisc pattern of an "immature" type, i.e., possibly indicating a relative understimulation of the gonads by gonadotrophic hormones, in vivo, was found in one of the four patients, i.e., the XYY-male, inspite of normal levels of gonadotrophic hormones in the peripheral circulation. Gametic output was found to increase significantly during the course of gonadotrophin substitution therapy, and the individual steroid metabolic pattern also changed drastically towards a more mature type subsequent to therapy.
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CAS 68-96-2 17Alpha-hydroxyprogesterone

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