Ostarine MK-2886 is a nonsteroidal Selective Androgen Receptor Modulator (SARM) with tissue-selective anabolic and androgenic pharmacological properties. It is also known in the scientific literature as enbosarm, GTx-024, or S-22.

This SARM was originally discovered in 1998 by James T. Dalton, Duane D. Miller, Karen A. Veverka, and their research teams at The Ohio State University, the University of Tennessee, and GTx, respectively. GTx has acquired the licensing rights from these research teams and further issued licenses to Merck & Co. for the development of MK-2886.

MK-2886 is one of the first SARMs to be synthesized and studied in both rats and primates, making it one of the most extensively studied SARMs.

In one study focusing on adult rats, specifically their fat cells or adipocytes, administration of MK-2886 Ostarine reduced the expression of fat-related hormones such as leptin and adiponectin mRNA. Researchers concluded that MK-2886 would likely have an effect similar to testosterone on the AR receptors, leading to a decrease in body fat in rats. Source

Another study showed that MK-2886 Ostarine also stimulates bone growth in rats. At the highest dose, 4 mg/kg, the test animals showed improved bone density, faster healing time and higher markers of bone growth hormones such as phosphorus and alkaline phosphatase.

Interestingly, all rats in the study group showed an increase in gastrocnemius muscle weight, even at the lowest dose of 0.04 mg/kg. Serum cholesterol levels were also reduced in this group, indicating an improved lipid profile. Source

In a subsequent study, similar results were observed; rats with clinically induced osteoporosis showed increased bone density when treated with moderate to high doses of MK-2866. Source

A third study assessed muscle growth in mice genetically modified to not have traditional androgen receptors. After removing the endogenous testosterone-producing cells, muscle breakdown began and treatment with MK-2886 was initiated. These mice showed muscle growth in androgen-sensitive muscles via an alternative pathway, different from that of the traditional androgen receptors. Source