RAD-140
Also known as: Testolone
Selective Androgen Receptor Modulator | Investigational SARM
Overview
RAD-140 (Testolone) is a nonsteroidal investigational selective androgen receptor modulator (SARM) originally developed by Radius Health, Inc. for the potential treatment of muscle wasting conditions and hormone receptor-positive breast cancer. It was designed to provide the anabolic benefits of testosterone, specifically increased lean muscle mass and bone density, while minimizing androgenic side effects in tissues such as the prostate and skin. RAD-140 has demonstrated a high degree of tissue selectivity in preclinical models, with an anabolic-to-androgenic ratio substantially greater than that of testosterone. It entered Phase 1 clinical trials for metastatic breast cancer (ER+/HER2-) and has shown preliminary safety and tolerability in that context. However, RAD-140 is not approved for any medical use by any regulatory agency. It remains a research compound, and its widespread use in performance and physique enhancement contexts is based almost entirely on preclinical data and anecdotal reports rather than completed clinical trials for those indications.
Key benefits
- Potent anabolic activity in muscle tissue with high oral bioavailability
- Tissue-selective action sparing the prostate and other androgen-sensitive organs
- No aromatization to estrogen (no estrogen-related side effects such as water retention or gynecomastia)
- No conversion to DHT (reduced risk of hair loss and prostate stimulation compared to testosterone)
- Long half-life (~60 hours) permitting convenient once-daily oral dosing
- Neuroprotective properties observed in preclinical models
- Increased lean body mass and reduced fat mass in preclinical studies
Mechanism of action
RAD-140 binds to the androgen receptor (AR) with high affinity and selectivity, functioning as a full agonist in muscle and bone tissue while exhibiting minimal agonist activity in the prostate and other androgen-sensitive tissues. This tissue selectivity is achieved through differential cofactor recruitment: upon binding to the AR, RAD-140 induces a conformational change that favors interaction with coactivators predominantly expressed in skeletal muscle and bone, rather than those prevalent in prostate or sebaceous glands. In preclinical studies, RAD-140 demonstrated potent anabolic effects on levator ani muscle mass comparable to testosterone, while showing significantly less stimulation of prostate weight. RAD-140 also crosses the blood-brain barrier and has demonstrated neuroprotective properties in in vitro models, reducing cell death caused by apoptotic insults in hippocampal neurons. At the molecular level, it activates AR-dependent gene transcription pathways involved in protein synthesis, nitrogen retention, and satellite cell proliferation in skeletal muscle. Importantly, RAD-140 does not undergo aromatization to estrogen and is not a substrate for 5-alpha reductase, meaning it does not produce estrogenic or DHT-mediated side effects. However, like all exogenous AR agonists, it suppresses endogenous testosterone production through negative feedback on the hypothalamic-pituitary-gonadal (HPG) axis.
Molecular data
- Type
- Nonsteroidal selective androgen receptor modulator (C20H16ClN5O2)
- Half-life
- ~60 hours
Indications
What the research community uses this compound for, with self-reported effectiveness.
Body Composition
Clinical / Investigational
Dosing protocols
Common protocols by delivery method. Adjust the curve below to model accumulation in your own cycle.
Delivery method
| Protocol | Dose | Frequency | Duration |
|---|---|---|---|
| — | 10 mg/day | Once daily | — |
| — | 15-20 mg/day | Once daily | — |
| — | 20-30 mg/day | Once daily | — |
Safety
Reported adverse effects, contraindications, and what to monitor on cycle.
Common side effects
- Testosterone suppression (dose-dependent, occurs in virtually all users by week 4-6)
- Liver enzyme elevation (ALT, AST increases reported in clinical and anecdotal data)
- Hair shedding (temporary, typically resolves after discontinuation)
- Headaches (most common in the first 1-2 weeks, often transient)
- Nausea (mild, usually with initial doses or on an empty stomach)
- Lipid disruption (HDL suppression, LDL elevation)
- Mild insomnia or sleep disturbance
- Reduced libido and mood changes related to testosterone suppression
Rare side effects
- Significant hepatotoxicity (clinical case reports of drug-induced liver injury at high doses or prolonged use)
- Severe testosterone suppression requiring extended PCT or medical intervention
- Aggression or mood instability
- Skin dryness or acne
- Elevated blood pressure
- Tendon or joint discomfort (related to drying effect from lack of estrogenic activity)
Contraindications
- Pre-existing liver disease or elevated liver enzymes at baseline
- Hormone-sensitive cancers (prostate cancer, certain breast cancers not being treated under clinical supervision)
- Pregnancy or potential pregnancy (teratogenic risk from androgen receptor agonism)
- Breastfeeding
- Age under 25 (incomplete endocrine system maturation and higher risk of HPG axis disruption)
- Concurrent use of hepatotoxic medications without medical supervision
- Known cardiovascular disease (insufficient safety data for this population)
Monitoring
- Total and free testosterone: baseline, mid-cycle (week 4-6), and post-cycle (2-4 weeks after PCT)
- Liver function panel (ALT, AST, bilirubin, ALP): baseline and every 4 weeks during cycle
- Lipid panel (total cholesterol, HDL, LDL, triglycerides): baseline and end of cycle
- Complete blood count: baseline and end of cycle
- Estradiol: baseline and post-cycle (to assess recovery)
- LH and FSH: post-cycle to confirm HPG axis recovery
References
Primary literature and clinical-trial data informing this entry.