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YK-11 is a synthetic steroidal selective androgen receptor modulator (steroidal SARM). It is a steroid compound based on 5-α-dihydrotestosterone (DHT), which is a gene-selective and partial agonist of the androgen receptor (AR). YK11 is so far the only SARM that is able to increase the expression of the activin binding protein Follistatin (FST), and right the induction of FST plays a key role in its anabolic effects. YK11 has chemical formula C25H34O6 and molecular mass 430.541 g·mol?1.

YK11 is a steroidal SARM (Selective Androgen Receptor Modulator). More specifically, it’s a Myostatin inhibitor. It’s considered to be one of the most powerful SARMs on the market and it’s actually comparable to certain steroids in its effectiveness.
YK11 is also a myostatin inhibitor (myostatin reduces our muscle mass), which means that you won’t be losing muscle while cutting and will very likely gain some instead, making it a great compound for cutting, lean bulking and especially body recomposition.

Well there are a few obvious benefits to taking a daily supplement designed to help build muscle.
First and foremost, YK-11 helps you grow more muscle in a smaller amount of time. YK-11 is a myostatin inhibitor which makes it easier for your body to develop more muscle.
In addition to more bulk, your muscles will become stronger from the production of follistatin. So as you can imagine, the stronger your muscles are the more you can do with them. Like steroids, YK-11 and other SARMs promote bone health and can make your bones stronger.
As mentioned earlier, YK-11 also helps with fat loss by replacing that fat with muscle.There are also claims that YK-11 helps boost libido and that it allows you to work out harder and longer. YK-11 can also help you retain the muscle that you have built.

YK11 is a novel steroidal compound that shows interesting gene-selective transcriptional activation of endogenous target genes. In human AR-positive MDA-MB 453 breast cancer cells, YK11 treatment induced FKBP51 mRNA expression similar to DHT treatment, though YK11 did not induce SARG mRNA expression, which DHT treatment can do. Selective induction of follistatin mRNA was the unique mechanism for YK11 activity because the induction was not shown by DHT. Thus, YK11 is a remarkable novel type of selective androgen receptor modulator[1].

Possible side effects of YK11 have not yet been scientifically investigated (at all). Theoretically, also the following side effects are not excluded:
Suppressed levels of natural Testosterone in the body (quite likely)
Increased risk of heart attack and stroke
Liver toxicity (due to the structure derived from DHT)
Can increase the progress of some cancer types (due to the increased expression of Follistatin)
The bodybuilding community on the Internet has experienced and reported with respect to YK11 some typical side effects, that occur with steroid use:
Mild testosterone suppression
Fatigue, low energy level
Aggression
Joint pain
Excessive hair loss
Mild acne

YK11 has a similar chemical structure to the dihydrotestosterone (DHT) from which it is derived, and both hormones YK11 and DHT bind to androgen receptors (AR). However, unlike DHT, YK11 does not induce the physical interaction between the NTD/AF1 and LBD/AF2 (known as the N/C interaction), which is required for full transactivation of the AR. In other words said, YK11 activates AR only partially, without the N/C interaction. Such partial (limited) activation of androgen receptors increases the catabolic activity in the body. However, YK11 also induces the expression of Follistatin (FST), an autocrine glycoprotein that is a potent inhibitor of the effects of Myostatin, a protein that brakes muscle growth. Thus, the resulting potent anabolic effect of YK11 is thought to be primarily due to the induction of expression of Follistatin, which blocks effects of Myostatin. The resulting anabolic activity of YK11 in C2C12 myoblasts is more potent than the anabolic activity of DHT.

[1] Tomofumi Yatsu. “Selective Androgen Receptor Modulator, YK11, Up-Regulates Osteoblastic Proliferation and Differentiation in MC3T3-E1 Cells.” Biological pharmaceutical bulletin 41 3 (2018): 394–398.