Roidipedia.Compound reference & reporting
06 AUG 2026
CompoundsSARM GLPG0492
SARMNon-steroidalSARMExperimental

GLPG0492

Also known as DT-200 · GLPG-0492

GLPG0492 (DT-200) is a non-steroidal selective androgen receptor modulator developed by Galapagos, studied preclinically for muscle-wasting conditions such as cachexia and Duchenne muscular dystrophy. It showed muscle-sparing effects in animal models with limited prostate stimulation, but has not completed human efficacy trials in the public record.

01 Overview

GLPG0492 was designed as an orally available SARM to counter muscle atrophy. In rodent models of disuse and disease-related muscle wasting it preserved muscle mass and function while producing weaker prostate effects than testosterone, consistent with the SARM tissue-selectivity concept.

Publicly available human clinical efficacy data are minimal, and the compound is not approved. Its appearance in the grey market is limited, and any human dosing is speculative. It remains essentially a preclinical research tool.

02 Mechanism

Non-steroidal androgen receptor agonist that selectively promotes anabolic signalling in skeletal muscle while sparing androgenic activity in prostate and seminal tissue in animal models.

03 Dosing

TierDoseRouteNotes
Anecdotal12–25 mg/dayOralNo validated human dose; values are speculative.

Ester comparison

EsterHalf-lifeInjection freq.Testosterone by mass

04 Effects

EffectMagnitudeEvidence
Muscle preservationPrevented loss of muscle mass and force in rodent atrophy models.Preclinical
Anti-cachectic effectReduced muscle wasting in disease models such as dystrophic mice.Preclinical

05 Side effects

EffectSeverityFrequencyEvidenceCountermeasures
HPTA suppressionAndrogen receptor agonism is expected to suppress endogenous testosterone; unquantified in humans.ModerateExpectedPreclinical
Uncharacterised human safetyNo published human toxicology or long-term data.ModerateUncharacterisedUnconfirmed

07 References

The selective androgen receptor modulator GLPG0492 attenuates muscle atrophyAmerican Journal of Physiology / preclinical literature, 2013

08 Discussion0 comments

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