The Androgen Receptor
How Testosterone and DHT Actually Signal in Cells
Evidence grade 5 of 5, Settled. Read how the Atlas grades evidence.
The written rationale for this grade is still being prepared.
- FDA
- Not a product (the molecular target of androgens)
Reference only. Not medical advice.
What can go wrong
The AR itself is not a treatment, but it is the target of consequential drugs. Androgen-receptor blockers are used in prostate cancer and can cause hypogonadal effects; complete androgen insensitivity (a loss-of-function AR mutation) shows that without a working receptor, even high testosterone has no masculinizing effect. Misunderstanding AR biology underlies many overstated supplement claims about 'boosting receptor sensitivity.'
This is something to take to a clinician. The Atlas can tell you what is known about the androgen receptor in general. It cannot tell you what is happening in your body, and the difference matters most for exactly the symptoms that bring people to this page.
The androgen receptor (AR) is the intracellular protein through which testosterone and its more potent metabolite dihydrotestosterone (DHT) exert their effects. When androgen binds, the receptor moves to the cell nucleus and regulates gene transcription. AR sensitivity varies between individuals, partly due to a polymorphic CAG-repeat length in the receptor gene, which helps explain why men with similar testosterone levels can have different responses. The AR is also the target of androgen-receptor-blocking drugs and the focus of SARM design.
The single molecular switch every androgen has to flip.
What people take it for
What it is taken for. Approval, where it exists, covers only some of these.
How it works
Testosterone and DHT diffuse into cells and bind the androgen receptor, displacing chaperone proteins. The activated receptor dimerizes, enters the nucleus, and binds androgen-response elements in DNA to switch target genes on or off. DHT binds the receptor more tightly and dissociates more slowly than testosterone, which is why 5-alpha-reductase conversion to DHT amplifies androgen action in tissues like skin, hair follicles, and prostate.
What it does to fertility
Androgen-receptor signaling within the testis is required for normal spermatogenesis; the AR is the mechanism through which intratesticular testosterone supports sperm production, which is why suppressing testosterone (and thus AR activation in the testis) impairs fertility.
What has to be monitored
The bloodwork this needs, and the reason it belongs with a clinician rather than a website.
- Clinical response relative to measured testosterone
- Consideration of AR-targeting medications in history
What people get wrong
Nothing recorded here yet. There is almost certainly something people get wrong about this one, and the blank space means we have not written it down, not that the record is clean.
Who profits, and who pushes back
Nobody is named here yet, because we have not done that work on this entry. Read that as unfinished. Somebody almost certainly sells this, and somebody almost certainly disputes it. Assume both until we have checked.
Set against the alternatives
Where most library entries discuss hormones and doses, the androgen receptor explains the downstream step that determines whether any of that testosterone actually does anything in a given tissue and a given individual.
At a glance
- Type
- Nuclear (intracellular) hormone receptor
- Ligands
- Testosterone and DHT (DHT binds more avidly)
- Variability
- CAG-repeat length influences sensitivity
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about The Androgen Receptor. A short entry is not a safe entry.
- Timeline. We have not built the dated record of research and regulatory events.
- Cost and market. We have not documented what it sells for or who sells it.
- Supply chain. We have not mapped where it is made.
- Who uses it. We have not documented the user groups.
- What could change. No forward-looking summary yet.
- Children and teenagers. We have not checked what is known about younger people.
- Where we land. We have not taken a position on this yet.
Sources
The studies below are named and described, but not linked. You cannot open them from here and check our reading against them, which means this page is our summary of the literature rather than a document you can verify. Weigh it accordingly until the links exist.
The studies that matter
Research on AR CAG-repeat polymorphismMultiple
Shorter CAG repeats are associated with greater androgen-receptor transcriptional activity, contributing to interindividual differences in androgen sensitivity
Characterization of complete androgen insensitivity syndromeFoundational
Demonstrated that nonfunctional androgen receptors prevent masculinization despite normal or high testosterone, establishing the AR as the obligatory mediator of androgen action