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Testosterone is the major binding partner of the androgen receptor (AR) and it serves a plethora of physiologic functions in humans: it is essential for maintaining sexual function, germ cell development, and the development of sex organs; it exerts dynamic effects in the skeletal muscle, fat, bone, and hematopoietic system via modulation of lipid, protein and carbohydrate metabolism; and it influences psychosexual and cognitive behaviors. Although natural testosterone deficiency in adult men is the most prevalent disorder related to AR signaling, the major stimulus for Selective Androgen Receptor Modulator (SARM) research and development has actually come from the tissue-specific anabolic effects these compounds exert on skeletal and muscle tissues preferentially, which suggests a wider range of uses.
Both men and women gradually and naturally lose muscle mass, strength and power as they age, and this widespread phenomenon has been traced to the loss of type II muscle fibers predominantly. These “fast-twitch” large-sized fibers are what produce the greatest cumulative and most responsive force profiles, which is absolutely essential for power activities like pushing, puling, lifting, running, jumping and balancing. Age-associated decline of muscle strength and mass increases the risk of skeletal fractures, limits mobility and independence, exacerbates physical disability and diminishes overall quality of life.
Economically, the physical decline and increased dependence that manifests in older individuals places a large burden on healthcare costs. Despite the high incidence of functional limitations and disability among those with decreased physical function and older individuals, there are nonetheless few therapeutic choices for the treatment of functional limitations for individuals with physical disability, or those seeking increased strength to mass ratios. As a result, there is a critical unmet need for anabolic therapies that can improve physical function and reduce the burden of disability or decreased muscle strength in a variety of individuals who require type II muscle fiber reinforcement. Amongst the innumerable candidate new-generation anabolic therapies that have benefitted from intensive research and development, SARMs offer the most exciting avenue for further study.
Exogenous testosterone supplementation (i.e. not produced by the body) has been shown to increase skeletal muscle mass and power in healthy men, in androgen-deficient middle-aged men, and in men with many chronic disorders. The anabolic effects of testosterone on skeletal muscle mass and strength are clearly related to testosterone dose and its circulating serum concentration. Moreover, the potential to achieve skeletal muscle remodeling, morphogenesis, and increased muscle mass and strength with androgen supplementation is substantial and obvious. Unfortunately, administration of exogenous androgens (such as testosterone) is strongly associated with a high frequency of dose-limiting adverse effects, such as blood cell count imbalance, peripheral limb swelling, prostate tissue dysregulation, and cardiovascular pathologies. This has been recognized for over 30 years, yet only recently has synthetic chemistry caught up with cell biology. Thus, therapeutic compounds such as SARMs that can reliably achieve anabolic effects on the skeletal muscle and bone absent the dose-limiting adverse effects associated with testosterone have become the holy grail of function-promoting anabolic therapies. The recognition of the fantastic promise of SARMs writ large has therefore spurred development of ever-increasing biochemical complexity that originated from parent compounds first synthesized a generation ago. Today, novel therapies for specific muscle mass-related goals and attendant physical ailments associated with suboptimal muscle strength, aging, and osteoporosis have resulted from ongoing pharmaceutical efforts all over the world.
The AR and its family of endogenous binding partners—the various natural androgens—are crucial for maintenance and morphogenesis of muscle tissue and bone matrix, secondary sexual organs, and development of other peripheral tissues. Although androgens are important for normal development secondary to various physiological processes, they can also unfortunately promote pathologies of the prostate, liver, and heart.
These downstream risks of exogenous testosterone therapy include dyslipidemia, benign prostatic hypertrophy (BPH), and cardiomyopathy. These pathological roles of testosterone and its 5α-reduced form (ie. DHT) limited their clinical viability and directly promoted the search for more tissue-selective binding partners of the AR that could activate the AR in the same fashion but only in selected tissues, while sparing the prostate, liver, and heart. Such molecules would provide the possibility to fully leverage the well-established therapeutic benefits of androgens. Most of the SARMs developed thus far are non-steroidal, and they demonstrate the capacity to activate AR in muscle and bone tissue, without a corresponding effect in the prostate or in seminal vesicles.
In related research, SARM development has also aimed to overcome undesirable effects of steroidal androgens in women who require increased muscle mass and strength secondary to a number of ailments. Obviously, females and males alike are both affected by osteoporosis, muscle wasting, and loss of muscle strength. Thus, “non-virilizing” SARMs (ie. those that don’t promote masculine-specific traits) could treat these pathological conditions in women without the unwanted masculine side-effects accompanying steroidal androgens. Until now, the recognized benefits of testosterone therapy in certain female populations are overshadowed by the risks of gaining masculine traits in addition to the poorly characterized cardiovascular risk. Moreover, recent clinical trials have demonstrated testosterone's ability to improve sexual function and muscle mass in older men, yet also substantiated concerns that testosterone's risk to the heart certainly offset its overall therapeutic benefits.
Since the discovery and origination of the first SARMs in early 1990s, several SARM-based structural scaffolds with divergent biochemistry have evolved and become increasingly decorated with additional molecules. The foundational preclinical evidence for the tissue-selectivity of SARMs was increased levator ani muscle weight in supplemented rats compared to control rats, despite only minimally increased prostate and seminal vesicle weight. This pioneering animal model, known as the Hershberger model, has become the primary mode for evaluating tissue selectivity throughout the history of SARM research. The efficacy of SARMs in levator ani muscle in males and pelvic floor muscles in females have also been tested ubiquitously and they formed the core experiments in early studies. Although the use of levator ani muscle as a proxy for anabolic activity in skeletal muscle has been criticized due to its unequal expression of AR, it nonetheless permitted a sensitive and linear measurement of anabolic effects over a useful range. After these early studies, newer experimental models to quantify raw muscle strength and power in animals and humans were developed to further test the efficacy of the burgeoning SARM compounds. Over the next 20 years, structure-activity relationship (SAR) studies were conducted on various SARMs that produced a handful of promising initial clinical candidates, with Enobosarm gaining the earliest investment in major pharmaceutical development. Excitingly, in addition to their effects on muscle mass and strength, numerous SARMs also demonstrated beneficial effects on skeletal tissue. As a result, several SARMs have been evaluated in several Phase I, Phase II, and Phase III clinical trials for a range of conditions including muscle wasting, loss of muscle strength, cancer treatment, and stress incontinence.
SARMs are also in development for indication in diseases where steroidal androgens were originally proposed as therapeutics. While the original focus of clinical development for SARMS was their use in combating muscle wasting, their use is now expanding to include many other indications, including what is perhaps the most exciting: the potential for prevention of breast and prostate cancers.
Adults over 35 years of age lose ~1% of their muscle mass each year. With life expectancy continuing to escalate, the sheer number of people with compromised muscle mass and attendant strength deficits during normal physical function has exploded in the last decade; to make matter worse, there is no strong clinical framework in place to stem the tide using preventative strategies. Age-related muscle loss currently has no tolerable treatment options with limited adverse effect profiles. Loss of muscle strength is a major cause of frailty and it carries an increase in physical disability as well as harm and mortality. The demographic that is most widely affected is adults over the age of 60 years of age, but younger adults are also at risk. Older adults, already at elevated risk to be deficient in muscle strength due to age-related physiological decline, are also at high risk to lose additional muscle due to co-morbid conditions that predictably arise during aging. SARMs are particularly relevant in this regard due to their tissue-selectivity and potential to provide therapeutic increases in muscle mass with reduced adverse effects.
Given the prevalent and growing use of corticosteroids to combat inflammation, allergies, and other health conditions, even young adults are vulnerable to corticosteroid-induced muscle loss. Although non-steroidal SARMs which spare muscle and bone—yet show significant anti-inflammatory effects—have been developed and tested preclinically, they have not successfully completed clinical trials, thus making steroidal corticosteroids the sole option for a variety of indications. Numerous SARMs have already been shown to be especially effective in multiple preclinical models of muscle loss, including glucocorticoid-induced muscle atrophy.
It was obvious early on that the capacity of SARMs to promote muscle and skeletal strength in preclinical models suggested that they may provide a fascinating therapeutic strategy to osteoporosis therapy. Currently, gradual bone loss due to age-associated osteoporosis is primarily treated with antiresorptive drugs such as bisphosphonates that prevent further breakdown of bone in the body. However, while well tolerated, these antiresorptive agents only prevent further bone loss and are unable to increase new bone mass. In preclinical models, AR-binding SARMs have successfully prevented bone loss in addition to increasing bone mineral density in large bones above baseline in a variety of experimental in vivo models. Thus, SARMs not only prevent loss of bone due to aging, but they also increase bone mineral mass and strength.
Overall, SARM development is rapidly expanding into many corners of life science research. While ongoing research is always necessary to fine tune and maximize the clinical benefits of emergent SARMs, there is nevertheless considerable evidence that already supports the safety, tolerability, and effectiveness of SARMS in the pursuit of gaining muscle mass and strength. Umbrella Labs is committed to the goal of fostering SARM research and development by providing a domestic source of SARM compounds for responsible R&D use.
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*The information herein is for educational and informational purposes only. THIS PRODUCT IS FOR RESEARCH USE ONLY. For use in animal studies, all research must be conducted with oversight from the appropriate Institutional Animal Care and Use Committee (IACUC) following the guidelines of the Animal Welfare Act (AWA).