Selective Androgen Receptor Modulator (SARM) RAD 140, also known as Testolone, is a synthetic compound investigated for its potential to stimulate muscle and bone growth. Due to its anabolic effects, RAD 140 has gained attention within performance-enhancing communities. The compound is not approved for human use, which creates uncertainty regarding its long-term safety profile. A major concern is whether RAD 140 carries a risk of inducing or promoting cancer. This article examines preclinical evidence regarding RAD 140’s potential link to cancer.
Defining RAD 140 and its Mechanism of Action
RAD 140 belongs to the class of non-steroidal compounds known as Selective Androgen Receptor Modulators (SARMs). It was developed by Radius Health as a potential treatment for conditions like muscle wasting and bone density loss. RAD 140 binds to the body’s androgen receptors (ARs), which are activated by hormones like testosterone and dihydrotestosterone (DHT).
The key difference between RAD 140 and traditional anabolic steroids is its tissue selectivity. Steroids activate ARs broadly, causing androgenic side effects in non-target tissues like the prostate and skin. RAD 140 is designed to preferentially activate ARs in muscle and bone tissue while exhibiting less activity in reproductive organs. This selectivity is achieved because, unlike testosterone, RAD 140 is not converted into more potent androgens like DHT or into estrogen by the aromatase enzyme. By selectively stimulating ARs in skeletal muscle, RAD 140 initiates anabolic signaling pathways that increase protein synthesis and cell growth.
Research Findings on Carcinogenic Potential
Cancer risk is complex due to the compound’s dual nature: it promotes muscle growth but was also studied as a potential anti-cancer agent. Preclinical investigations have provided specific insights into how RAD 140 interacts with various cell types. The most definitive anti-cancer finding relates to hormone-sensitive breast cancer models.
Studies demonstrated that RAD 140 acts as an AR agonist in androgen and estrogen receptor-positive (AR/ER+) breast cancer cells, inhibiting their growth. This effect is distinct from traditional treatments, as RAD 140 was found to regulate AR target genes while actively suppressing estrogen receptor signaling. This suggests that in certain hormone-dependent cancers, the compound may have a therapeutic, rather than a carcinogenic, effect.
The risk of prostate cancer, a common concern with traditional androgens, appears reduced in animal models receiving RAD 140. In rat studies, RAD 140 showed partial efficacy on the prostate and seminal vesicles compared to testosterone propionate. RAD 140 did not stimulate prostate tissue to the same extent as testosterone, even at high doses. This limited androgenic effect on the prostate, a major site of androgen-driven cancer, is a primary feature of the compound’s selective action.
Although the compound completed preclinical toxicology assessments in rats and monkeys, comprehensive, long-term two-year rodent carcinogenicity bioassays have not been published in the public domain. The current data primarily focuses on the compound’s tissue-selective profile and therapeutic potential in specific cancer models. Until full toxicology data becomes publicly available, or long-term human data exists, conclusive statements regarding the promotion of tumor growth in other non-prostate tissues, such as the liver or colon, cannot be made.
Regulatory Status and Limitations of Long-Term Data
RAD 140 is an investigational drug that has not received approval from regulatory bodies like the U.S. Food and Drug Administration (FDA) for human therapeutic use. The compound remains in the early stages of development and is currently classified as a research chemical. This designation signifies a lack of long-term human safety and efficacy data necessary for clinical approval.
The absence of definitive, long-term human safety data is a direct result of the compound never completing Phase 3 clinical trials. Clinical trials are designed to systematically evaluate safety, dosing, and efficacy over extended periods in large human populations. Without these completed trials, the true incidence of rare or delayed side effects, including cancer, remains unknown.
Instead of being administered under medical supervision, RAD 140 is often illegally sold and purchased on the black market for performance enhancement. This unregulated environment means users are consuming a substance with unknown purity, potency, and long-term effects. Furthermore, the World Anti-Doping Agency (WADA) prohibits RAD 140 use in competitive sports due to its anabolic properties.
Other Significant Non-Cancer Safety Concerns
While the cancer risk remains a long-term question, other safety concerns related to RAD 140 use are more immediate and frequently documented. One of the most common adverse effects is hepatotoxicity. Case reports have linked the use of RAD 140 to drug-induced liver injury, characterized by elevated liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST).
The pattern of liver injury often observed is cholestatic, a condition frequently associated with anabolic steroid use. Elevated bilirubin levels and jaundice have been noted in users who stopped taking the compound, with symptoms resolving only after cessation. This suggests that RAD 140 can place stress on the liver’s function.
Another side effect is the suppression of the body’s natural hormone production. RAD 140 disrupts the hypothalamic–pituitary–gonadal (HPG) axis, leading to a decrease in endogenous testosterone levels. In preclinical primate models, testosterone levels dropped by about 50% after a 28-day course, even at low dosages. This hormonal suppression often necessitates post-cycle therapy to help the body restore its natural testosterone production.