RESEARCH MONOGRAPH · KDC-MN-386
Testosterone (Research)
Testosterone is the principal androgen in humans, made from cholesterol in the testes (men) and ovaries plus adrenals (women). It is the foundational compound of androgen pharmacology and the active ingredient in essentially all testosterone replacement therapy plus the backbone of most non-medical anabolic steroid stacks. It binds the androgen receptor directly and is also converted on the fly into dihydrotestosterone (more potent androgen) by 5-alpha-reductase, and into estradiol by aromatase. Sold as cypionate, enanthate, propionate, undecanoate, plus gels and patches, with each ester releasing testosterone over different timescales. Schedule III in the US. The reference androgen receptor agonist for nearly all related research. Not stocked by Kodiac. This monograph is provided for research and educational reference.
Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.
Endogenous androgen / anabolic-androgenic steroid
The principal endogenous androgen; the foundational compound of androgen pharmacology and the active component of TRT and many AAS regimens.
Abstract
Testosterone (17-beta-hydroxyandrost-4-en-3-one; CAS 58-22-0; molecular formula C19H28O2; molecular weight 288.42) is the principal endogenous androgen, biosynthesized from cholesterol via pregnenolone and progesterone in Leydig cells of the testis (males) and theca cells, ovary, and adrenal cortex (females). The compound is the prototype androgen receptor agonist and the foundation of androgen pharmacology. Pharmacologically, testosterone binds AR (Ki approximately 0.5 nM) and is converted to dihydrotestosterone (DHT) by 5-alpha-reductase (more potent AR agonist) and to estradiol by aromatase (estrogen receptor agonist). Approved as testosterone replacement therapy in male hypogonadism via various ester formulations: cypionate, enanthate, propionate, undecanoate (oral and depot), gels and patches. Schedule III in the US under the CSA. The compound is the foundation of most anabolic-androgenic steroid (AAS) regimens used non-medically for muscle building. Plasma half-life of native testosterone is short (1 to 2 hours); ester formulations release the parent compound over days. Used as the canonical AR agonist in research.
Mechanism of action
Androgen receptor agonist; converted to DHT (5-alpha-reductase) and estradiol (aromatase) for tissue-specific effects. Ester formulations extend release.
Reported research dose ranges
Reported research dose ranges vary across the published literature.
References
- Bhasin S, et al. Testosterone therapy in men with hypogonadism: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab 2018.
- Kicman AT. Pharmacology of anabolic steroids. Br J Pharmacol 2008.
- Mooradian AD, et al. Biological actions of androgens. Endocr Rev 1987.
Read the full monograph
Available as a research-use-only PDF download.
The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.
FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.