Anadrolus (Oxymetholone)

About the Product

Anadrolus is a research compound from Driada Medical, containing Oxymetholone. Oxymetholone is a synthetic anabolic-androgenic steroid (AAS) and a 17α-alkylated derivative of dihydrotestosterone (DHT). Its chemical formula is C₂₁H₃₂O₃, with a molecular weight of 332.5 g/mol, a CAS number of 434-07-1, and a logP of 4.22.

The compound is characterized by two key structural features:

• 17α-methyl group: Provides steric hindrance against hepatic metabolism, enabling oral bioavailability in research models, but is also associated with significant hepatotoxic effects.

• 2-hydroxymethylene modification: Distinguishes it from other AAS and contributes to its unique receptor binding profile.

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

• Product Name: Anadrolus (Oxymetholone)

• Brand: Driada Medical

• Form: Solution for research applications

• CAS: 434-07-1

• For Research Use Only.

Research Applications & Mechanism of Action

• Androgen Receptor Agonist with Low Binding Affinity: Oxymetholone functions as an agonist at the androgen receptor (AR). Research shows it has a low binding affinity for the AR but is a potent activator of AR-mediated signaling. It demonstrates an interaction energy of -1350.53 kcal/mol and a predicted binding free energy (ΔG) of -8.83 kcal/mol (compared to -1400.63 and -10.06 for testosterone).

• Erythropoiesis Stimulation: Oxymetholone enhances the production and urinary excretion of erythropoietin in research models, stimulating erythropoiesis in anemias due to deficient red cell production.

• Protein Anabolism: The primary mechanism is the ability to increase protein synthesis and enhance nitrogen retention in muscle cells via androgen receptor activation.

• Steroidogenesis Research: Studies demonstrate that oxymetholone decreases corticosteroid but increases dehydroepiandrosterone (DHEA) biosynthesis in H295R cells, suggesting CYP21A2 inhibition.

• Oxidative Stress Research: Animal studies show that oxymetholone significantly increases oxidative stress markers (MDA) while depleting antioxidant defenses (GSH, catalase, SOD), and upregulates pro-inflammatory genes (TNF-α, NF-κB, STAT3) while downregulating antioxidant genes (Nrf2, CAT, SOD).

• Hepatotoxicity Research: Oxymetholone demonstrates direct toxicity to hepatocytes in vitro at 1 × 10⁻⁴ M concentrations, causing significant increases in LDH release (plasma membrane damage), decreased cell viability, and glutathione depletion within 2-6 hours.

Research & Scientific Background

• Chemical Background: Oxymetholone is an orally active 17α-alkylated DHT derivative with an androgenic:anabolic ratio of 1:1 to 1:3 in rodent models. The 17α-methyl group confers oral bioavailability but is also responsible for the compound's narrow therapeutic index.

• Clinical Context: Clinically, oxymetholone (Anadrol-50) is FDA-approved for the treatment of anemias caused by deficient red cell production, including acquired aplastic anemia, congenital aplastic anemia, myelofibrosis, and hypoplastic anemias due to myelotoxic drugs.

• Androgen Receptor Binding Research: Computational studies demonstrate that oxymetholone is predicted to bind to multiple nuclear hormone receptors beyond the androgen receptor, including the estrogen receptor, thyroid receptor, and orphan nuclear receptors. This suggests potential non-specific binding that may contribute to its side-effect profile.

• Hepatotoxicity Research: The compound has known boxed warnings for peliosis hepatitis (liver tissue replaced with blood-filled cysts), liver cell tumors, and adverse blood lipid changes. In human case reports, severe jaundice (bilirubin up to 21.9 mg/dL) and hepatic coma have occurred within 6-8 weeks of therapy. The direct toxicity of the 17α-alkylated structure has been confirmed in primary rat hepatic cell cultures, with oxymetholone showing significant LDH release and cell viability decreases at 1 × 10⁻⁴ M for 4 and 24 hours, and glutathione depletion within 2, 4, and 6 hours.

• Oxidative Stress & Inflammatory Research: Recent rodent studies demonstrate that oxymetholone exposure increases serum ALT, AST, urea, creatinine, and MDA while depleting GSH. It upregulates pro-inflammatory genes (TNF-α, NF-κB, STAT3) and downregulates antioxidant genes (Nrf2, CAT, SOD), with histopathological examination revealing extensive liver and kidney damage. Similar findings in mice (5 mg/kg/day for 30 days) showed significant decreases in total antioxidant capacity and catalase activity, and increased lipid peroxidation.

• Genetic Variability Research: While direct studies on oxymetholone pharmacogenomics are limited, the field of pharmacogenomics indicates that genetic variations in drug-metabolizing enzymes (e.g., CYP3A4, UGTs) can significantly influence compound response and toxicity. The compound's distinct CYP21A2 inhibition profile and receptor binding dynamics provide a basis for investigating genetic factors affecting individual susceptibility.