RAD 150 Before and After: The Reported Effects & Risks

RAD 150 has no published human clinical trials, no approved medical use, and no peer-reviewed “before and after” data. What circulates online under that name is an esterified form of RAD 140, a selective androgen receptor modulator (SARM) that itself remains experimental. The “before and after” reports you find on forums and social media are entirely anecdotal, and the risks that do show up in the limited research on its parent compound are more serious than the typical gym-culture narrative suggests.

What RAD 150 Actually Is

RAD 150, sometimes sold as TLB-150 benzoate, is RAD 140 with a benzoate ester group chemically attached. Esterification is a well-known strategy in pharmacology for extending how long a drug stays active in the body. By attaching an ester to the parent molecule, the compound is absorbed more slowly and takes longer to break down. In theory, this means RAD 150 provides a longer-lasting effect per dose than RAD 140. In practice, nobody has tested this in controlled human studies. The ester concept is borrowed from how injectable testosterone variants work (testosterone enanthate and testosterone cypionate are esterified forms of testosterone), but that parallel does not mean RAD 150 has been validated the same way.

Once the ester group is cleaved off in the body, what remains is RAD 140. So the pharmacological activity of RAD 150 should, in principle, mirror that of RAD 140. This means the preclinical research on RAD 140 is the closest thing to evidence we have for what RAD 150 does biologically. But “closest thing” is doing a lot of work in that sentence. Animal pharmacokinetics do not translate cleanly to humans, and the ester modification itself introduces unknowns about absorption, metabolism, and tissue distribution that have not been characterized.

What “Before and After” Reports Actually Describe

If you search for RAD 150 before-and-after accounts, you will find them almost exclusively on Reddit, bodybuilding forums, and social media. These reports typically describe cycles lasting four to eight weeks, with users claiming increased lean muscle mass, improved workout endurance, a “harder” or more vascular appearance, and modest fat loss. Some users post physique photos showing visible changes over the course of a cycle.

The problem with treating these accounts as evidence is not that every single one is fabricated. Some users may genuinely be experiencing changes. The problem is that you cannot separate what the compound did from what training, diet, creatine, sleep, lighting in the photo, and the placebo effect contributed. Users running RAD 150 cycles are typically also training hard, eating in a caloric surplus or controlled deficit, and highly motivated. Any of those factors alone can produce visible changes over two months. Without a control group doing the same training and eating the same food without taking the drug, the “before and after” comparison is essentially meaningless as pharmacological evidence.

Physicians are increasingly aware that patients are turning to social media for information about SARMs, and that adverse events from these compounds are likely underreported in the medical literature compared to what users actually experience.1Journal of Medical Internet Research. Self-Reported Side Effects Associated With Selective Androgen Receptor Modulators: Social Media Data Analysis The enthusiasm you see online is shaped by survivorship bias: people who had a good experience post about it, and people who felt terrible or got bloodwork back showing liver damage are less likely to share publicly.

What Preclinical Research Shows About RAD 140

Since RAD 150 converts to RAD 140 in the body, the animal data on RAD 140 is the best available window into its biological effects. RAD 140 was originally developed as a potential treatment for muscle-wasting conditions and osteoporosis. In preclinical studies, it stimulates increases in muscle weight at lower doses than those needed to enlarge the prostate, which is the core selling point of SARMs over traditional anabolic steroids: tissue selectivity.2Open Access Journal of Reproductive System and Sexual Disorders. Selective Androgen Receptor Modulators (SARMs): A Mini-Review

A study in young healthy rats found that RAD 140 could stimulate muscle hypertrophy. Rats given RAD 140 without any additional exercise stimulus showed significantly increased muscle fiber cross-sectional area compared to untreated controls. When RAD 140 was combined with a muscle overloading protocol (essentially forced exercise), muscle weight increased markedly, though the increase was not statistically different from the overloading protocol alone.3PubMed Central. Preclinical assessment of the selective androgen receptor modulator RAD140 to increase muscle mass and bone mineral density In other words, the drug appeared to help muscle grow on its own, but adding it on top of hard exercise did not produce a clearly larger effect than the exercise by itself. That is a finding worth sitting with if you are considering running a cycle. The animal data does not straightforwardly support the idea that RAD 140 will amplify your training results in a dramatic way.

These are rat studies. Rats metabolize drugs differently, respond to androgens differently, and the doses used are not directly translatable to human doses. No published, peer-reviewed study has measured what RAD 140 or RAD 150 does to human muscle tissue, human body composition, or human athletic performance in a controlled setting.

Liver Toxicity Is a Real and Documented Risk

This is where the risk profile gets concrete. In a study that tracked liver biomarkers in subjects taking RAD 140, elevations in the liver enzyme AST occurred in about 59% of subjects, with roughly a quarter of those reaching grade 3 or 4 severity (meaning levels more than five times the upper limit of normal). ALT elevations appeared in about 45% of subjects, again with about a quarter hitting severe grades. Total bilirubin, another marker of liver stress, was elevated in about 27% of subjects. Four subjects had ALT elevations severe enough to be classified as dose-limiting toxicities, and two had AST elevations at that level, though all were reported as reversible.4Journal of Clinical and Translational Hepatology. Selective Androgen Receptor Modulators: An Emerging Liver Toxin

Those numbers are striking. More than half of users showing elevated AST is not a minor footnote. And while the elevations were reversible in that study, the broader SARM literature includes published case reports of drug-induced liver injury with cholestatic or hepatocellular damage and jaundice. Since 2020, at least 20 such adverse event reports have appeared in the medical literature, most involving liver injury from SARM use.5PubMed Central. Selective androgen receptor modulator use and related adverse events including drug-induced liver injury: Analysis of suspected cases These case reports are the tip of the iceberg, since most SARM users never get bloodwork done and never see a doctor about their cycle.

RAD 150 adds another layer of uncertainty here. The ester group has to be metabolized somewhere, and the liver is the organ most likely handling that job. Whether the esterified form is harder on the liver than plain RAD 140 is unknown because nobody has studied it. You are essentially beta-testing a modified research chemical on your own liver.

Hormonal Suppression and What Recovery Looks Like

SARMs suppress your body’s natural testosterone production. This happens through the same feedback mechanism that anabolic steroids trigger: when the androgen receptor is being activated by an external compound, the brain’s signaling system dials down its own production of luteinizing hormone (LH), which in turn reduces testosterone output from the testes. The degree of suppression varies by compound, dose, and cycle length, but the effect is well-established for the SARM class and is one of the primary reasons users plan “post-cycle therapy” after stopping.

After stopping exogenous androgens, the hormonal axis needs time to restart. In a study of men who had used anabolic compounds, LH levels during use dropped to a median of about 0.2 mIU/mL, far below normal. After three months of cessation, median LH recovered to about 4.1 mIU/mL, and testosterone levels rose from a depressed median to around 4.55 ng/mL. However, about one in five men in that study still had testosterone below 3.4 ng/mL at the three-month mark, qualifying as poor recovery.6PubMed. Peculiarity of recovery of the hypothalamic-pituitary-gonadal axis, in men after using androgenic anabolic steroids Recovery was strongly correlated with how long the compounds were used, how high the doses were, and what type of androgens were involved.

The broader clinical picture confirms that spontaneous recovery happens for the majority of individuals within months after cessation, but prolonged or even permanent post-androgen hypogonadism has been described in the literature.7PubMed Central. Post-cycle therapy after androgen abuse: a narrative review of mechanisms, evidence, and clinical perspectives Another review notes that while endogenous testosterone production often recovers within three months, permanent suppression is a documented possibility.8PubMed. Management of symptoms of hypogonadism in patients after androgen abuse

The practical takeaway: if you run a RAD 150 cycle, you should expect at least some suppression of your natural testosterone. Most users will recover, but a meaningful minority take months to bounce back, and a small fraction may not fully recover. The online framing that SARMs are “milder” than steroids on the hormonal axis is at best an oversimplification, because the suppressive mechanism is fundamentally the same.

Tendon and Connective Tissue Risks

A commonly overlooked side effect of androgen use, whether steroids or SARMs, involves tendons and ligaments. Androgens drive muscle growth, but they can simultaneously weaken the connective tissues that anchor muscles to bone. High-dose androgen use disrupts collagen balance and increases injury risk by creating a mismatch between rapidly growing muscle strength and tendon resilience that has not kept pace.9PubMed Central. Impact of Anabolic Steroids on Tendons: A Narrative Review

Animal research reinforces this. Rats given androgens while undergoing physical exercise showed impaired tendon remodeling due to suppression of the enzymes responsible for tissue repair, increasing the potential for tendon injury.10PubMed. Androgenic-anabolic steroids associated with mechanical loading inhibit matrix metallopeptidase activity and affect the remodeling of the achilles tendon in rats This is particularly relevant for RAD 150 users because the whole point of taking it is to train harder and lift heavier. If the compound is making your muscles stronger while simultaneously making your tendons more fragile, you are setting yourself up for the kind of sudden tendon tear that ends a training career. Users rarely mention this risk in before-and-after threads, but orthopedic surgeons see the consequences.

You Might Not Even Be Taking What You Think

Even if you have decided the risk-benefit tradeoff is acceptable, there is a more fundamental problem: the product in the bottle may not be what the label says. A landmark analysis of 44 products marketed and sold online as SARMs found that only about half actually contained a SARM at all. About 39% contained a completely different unapproved drug. In roughly 9% of products, no active compound was detected whatsoever. And in only 41% of the products tested did the amount of active ingredient match what was listed on the label.11PubMed Central. Chemical Composition and Labeling of Substances Marketed as Selective Androgen Receptor Modulators and Sold via the Internet

A separate analysis of SARM supplements available to UK consumers found similar problems: some products contained no active ingredients at all, others contained undeclared prohibited substances, and where SARMs were detected, the actual concentrations did not match the label.12Drug Testing and Analysis. Analysis of supplements available to UK consumers purporting to contain selective androgen receptor modulators This means that any individual “before and after” experience with RAD 150 might actually reflect the effects of a different compound entirely, or a sub-therapeutic dose of what was expected, or an overdose of something unlisted.

RAD 150 is even more vulnerable to this problem than better-known SARMs like ostarine or LGD-4033, because it is a niche compound with a smaller market, which means less third-party testing, fewer consumer reports to cross-reference, and less incentive for suppliers to invest in quality control. If you are reading a glowing before-and-after review of RAD 150, you have no way of knowing whether the reviewer actually consumed RAD 150, some other SARM, a prohormone, or a capsule of filler.

The “Tissue Selectivity” Promise Has Limits

The marketing pitch behind SARMs is that they activate androgen receptors in muscle and bone while largely sparing the prostate, skin, and other tissues that cause problems with traditional steroids. RAD 140 does appear to show a favorable ratio of anabolic to androgenic activity in rats, stimulating muscle growth at doses lower than those needed to enlarge the prostate.2Open Access Journal of Reproductive System and Sexual Disorders. Selective Androgen Receptor Modulators (SARMs): A Mini-Review That selectivity is real in preclinical models, but it is not absolute, and it has never been confirmed in long-term human use.

The liver toxicity data already discussed shows that “tissue selective” does not mean “side-effect free.” The hormonal suppression data shows that selectivity at the receptor level does not prevent whole-system consequences. And the doses users take in real-world cycles often far exceed the doses used in preclinical research, which may obliterate whatever selectivity the compound has at therapeutic levels. A compound that is tissue-selective at 10 mg may behave much more like a blunt androgen at 30 mg. Users experimenting with their own dosing protocols have no pharmacokinetic data to guide those decisions.

What Bloodwork Typically Reveals During a Cycle

Users who do get bloodwork during a RAD 150 cycle commonly report suppressed LH and testosterone levels, elevated liver enzymes (ALT and AST), and shifts in lipid profiles. The preclinical profile of RAD 140 includes lowering of LDL, HDL, and triglycerides.2Open Access Journal of Reproductive System and Sexual Disorders. Selective Androgen Receptor Modulators (SARMs): A Mini-Review On paper, lower LDL sounds like a benefit, but the simultaneous drop in HDL (the “protective” cholesterol) shifts the ratio in an unfavorable direction, which is a pattern also seen with anabolic steroids and is associated with increased cardiovascular risk over time.

If you are going to use RAD 150 despite the unknowns, getting bloodwork before, during, and after a cycle is the bare minimum for managing risk. At a minimum, you want a complete metabolic panel covering liver enzymes, a lipid panel, and a hormone panel including total testosterone, free testosterone, and LH. Many users skip this step because the results are inconvenient or because they do not want to explain to their doctor what they are taking. That reluctance is understandable but dangerous, especially given how common liver enzyme elevations appear to be.

Why No Legitimate “Before and After” Study Exists

RAD 140 entered a phase 1 clinical trial as a potential cancer treatment, but that trial focused on safety and tolerability at escalating doses in patients with advanced breast cancer, not on body composition or athletic performance in healthy people. No pharmaceutical company has funded or published a trial measuring what RAD 140 or RAD 150 does to muscle mass, strength, or body fat in healthy volunteers in a placebo-controlled design. The compound is not approved by any regulatory agency for any use. It is classified as an investigational drug, and selling it for human consumption is illegal in many jurisdictions.

This means every “before and after” claim exists in a complete evidence vacuum. Not a partial vacuum where we have small studies and need bigger ones. A complete vacuum where no controlled human study of the relevant outcomes has ever been conducted. The preclinical animal data is encouraging enough to justify further research, which is why pharmaceutical interest in RAD 140 exists at all. But the gap between “promising in a rat model” and “safe and effective in humans” is enormous, and it is a gap that has swallowed many drug candidates. Users who take RAD 150 based on forum reports are skipping ahead of the science by years or possibly decades.

The Ester Does Not Make It Safer

Some vendors market RAD 150 as an upgrade over RAD 140, implying that the ester modification somehow makes it smoother, less suppressive, or easier on the body. There is no pharmacological basis for this claim. Esterification affects how quickly a drug is absorbed and how long it stays in circulation. It does not change the fundamental activity of the parent molecule once the ester is cleaved. If RAD 140 suppresses your testosterone, RAD 150 will too. If RAD 140 raises your liver enzymes, RAD 150 will too. The extended half-life might actually make side effects harder to manage, because the compound stays in your system longer after each dose. If you develop a problem, you cannot simply stop and have it clear quickly.

The ester also means there is an additional metabolic step involved, introducing at least one more variable that has never been characterized in humans. No published data describes how efficiently the benzoate ester is cleaved in human tissue, what intermediate metabolites are produced, or whether those intermediates have their own biological activity. This is a genuinely unknown aspect of the compound’s pharmacology, and it represents a risk that does not exist with the parent molecule.