Provironus (Mesterolone)

About the Product

Provironus is a research compound from Driada Medical, containing Mesterolone. Mesterolone is a synthetic, orally active androgen and a derivative of dihydrotestosterone (DHT). Its chemical formula is C₂₀H₃₂O₂, with a molecular weight of 304.47 g/mol.

The compound is characterized by a 1α-methyl group on the DHT backbone. This structural modification prevents the metabolism of the steroid to estrogen (aromatization), distinguishing it from testosterone and its derivatives. This feature, combined with its oral bioavailability and relatively good hepatic tolerability, makes it a valuable research tool for studying androgen receptor (AR) signaling.

The product is intended for laboratory research use only and features an integrated QR code on the packaging for detailed product verification.

• Product Name: Provironus (Mesterolone)

• Brand: Driada Medical

• Form: Solution for research applications

• CAS Number: 1424-00-6

• For Research Use Only.

Research Applications & Mechanism of Action

• Androgen Receptor Agonist: Mesterolone functions as an agonist at the androgen receptor (AR). Its relative binding affinity (RBA) is approximately 25 when compared to the synthetic androgen methyltrienolone (MT, RBA=100) in rat prostate tissue. For reference, DHT has an RBA of 46 in the same assay.

• Non-Aromatizable Androgen: Due to its 1α-methyl group, mesterolone is not a substrate for the aromatase enzyme and therefore does not convert to estrogen. This makes it a valuable tool for studying pure androgenic effects without the confounding variables of estrogenic activity.

• High SHBG Affinity: Mesterolone exhibits an exceptionally high affinity for sex hormone-binding globulin (SHBG), approximately 4 times that of DHT. In research models where SHBG expression is relevant, this property can be used to study the displacement of endogenous testosterone and consequent alterations in the free fraction of the hormone.

• Steroidogenesis Research: Recent research has shown that mesterolone can interfere with adrenal steroidogenesis. Studies in H295R cells demonstrate that mesterolone increases mineralocorticoid production (aldosterone and 11-deoxycorticosterone) while decreasing adrenal androgen production, suggesting an indirect inhibition of CYP17A1 function. This positions the compound as a relevant tool for studying steroidogenic disturbances and their link to cardiovascular effects.

• Hormonal Regulation Research: Unlike many other androgens, mesterolone at therapeutic doses does not significantly suppress the release of gonadotropins (LH and FSH) in healthy men, likely due to its low central activity. This profile allows researchers to study its effects without the complete suppression of the hypothalamic-pituitary-gonadal (HPG) axis often seen with other AAS.

• Pharmacokinetic Studies: Mesterolone is rapidly and almost completely absorbed after oral administration in the 25-100 mg dose range, reaching peak serum concentrations in approximately 1.6 hours. Its absolute bioavailability is around 3% due to extensive first-pass metabolism. It is highly protein-bound (98%), with 58% binding to SHBG and 40% to albumin. The serum elimination half-life is 12-13 hours.

Research & Scientific Background

• Chemical Background: Mesterolone is a DHT derivative with a methyl group at the C-1 position. Its structural features confer oral bioavailability while the lack of 17α-alkylation contributes to a better hepatic tolerability profile compared to other orally active androgens.

• Clinical Context: Mesterolone (Proviron) has been clinically indicated for the treatment of conditions related to androgen deficiency in men, including hypogonadism, infertility, and disturbances of libido and potency.

• Androgen Receptor Binding Research: The relative binding affinity (RBA) of mesterolone has been characterized in competitive binding assays. Data indicates an RBA of 25 (vs. methyltrienolone) and ~400 (vs. DHT in SHBG binding). This places its AR affinity between testosterone and DHT, but its SHBG affinity is markedly higher.

• Adrenal Steroidogenesis Research: A study profiling the effects of various AAS on adrenal steroidogenesis identified mesterolone as a compound that increases mineralocorticoid biosynthesis (aldosterone and 11-deoxycorticosterone) while decreasing adrenal androgen production in H295R cells. The mechanism did not involve direct CYP17A1 inhibition or altered gene expression of key steroidogenic enzymes (3β-HSD2, CYP17A1, CYP21A2, CYP11B1, CYP11B2), suggesting an indirect effect potentially involving post-translational modification or impaired protein stability. This has been linked to the potential for promoting hypertension and cardiovascular diseases through mineralocorticoid excess.

• Drug Metabolism: Mesterolone is rapidly metabolized to 1α-methyl-androsterone (55-70% of metabolites) and 1α-methyl-5α-androstane-3α,17β-diol (~3%). No metabolic conversion to estrogens or corticoids has been observed. Approximately 80% of the dose is excreted in urine as metabolites and 13% in feces.

• Genetic Variability Research: While direct pharmacogenomic studies on mesterolone are limited, its high affinity for SHBG suggests that polymorphisms in the SHBG gene (which are common and associated with SHBG levels) may influence its biological activity by affecting the free fraction of the compound.