Common (>10% users at typical 10-15 mg/day):

• HPG suppression — universally reported, severity in community bloodwork tends to exceed RAD-140 and LGD-4033 at comparable doses. T drops to single-digit-percent-of-baseline reported in a subset of users.
• Mild-to-moderate ALT/AST elevation — reported in essentially all users with documented bloodwork by week 4-6. Magnitude variable; some users see 2-3× ULN, others stay within normal range with TUDCA/NAC support.
• HDL crash — substantial HDL reduction reported, often more aggressive than other SARMs. LDL frequently rises in parallel.
• Lethargy / fatigue — particularly in the back half of cycles and into PCT.
• Libido changes — initial frontload effect (up or down) followed by suppression-related crash.

Less common (1-10%):

• Cholestatic hepatotoxicity / drug-induced liver injury (DILI) — clinically apparent jaundice, dark urine, pruritus, marked LFT elevation. Published case reports exist within the broader SARM hepatotoxicity literature with YK-11 attributed; counts are low (<10 published cases identifiable as YK-11-specific) but the structural argument predicts higher true incidence. Most cases resolve on cessation with hepatology supportive care; recovery time 4-12 weeks.
• Hypertension — mild-moderate BP elevations reported, presumed AR-mediated water/sodium retention.
• Headaches — reported in a meaningful subset, sometimes daily.
• Aggression / irritability — reported, less consistently than with RAD-140.
• Sleep disruption — reported, often dose-dependent.
• Acne / oily skin — less common than with full AAS but present in some users.
• Visual disturbances — uncommon; cross-class SARM phenomenon.
• Hair shedding — DHT-derivative scaffold makes scalp-AR activation plausible; community reports mixed.

Rare-serious (<1% but worth knowing):

• Severe DILI requiring hospitalization or transplant evaluation — case reports exist within the SARM literature broadly; YK-11-specific attribution is muddled by polysubstance use and product-identity uncertainty, but the structural hepatotoxicity class membership predicts this outcome at non-negligible rates with extended use.
• Persistent hypogonadism — incomplete HPG-axis recovery reported in a subset of users; predictors poorly characterized; treatment is prolonged SERM + HCG or eventually clinical TRT.
• Hippocampal oxidative stress / mitochondrial dysfunction — extrapolated from Dahleh 2023 rat data; human translation unverified but mechanistically plausible. For a brain-priority user this risk vector matters even if the absolute incidence is low.
• Counterfeit / contamination toxicity — products sold as "YK-11" have been identified in independent forum testing as RAD-140, methylstenbolone, or other compounds. The toxicity then reflects whatever is actually in the bottle, which may include 17α-alkylated AAS, prohormones, or unrelated chemicals.
• WADA AAF / banned-list positive — long detection window via glucuronidated metabolites detectable >48h post-dose; longer-term metabolites identified in Piper 2018 work suggest multi-week detection windows.

Specific watch periods:

• Weeks 4-8: First likely hepatotoxicity onset window; LFT panel mandatory at week 4.
• End of cycle and into PCT (week 6-12+): HPG-axis recovery monitoring. Total T, LH, FSH, sensitive E2 at +2, +4, +6, +8 weeks post-cycle.
• Lipid panel at week 6 on cycle and 6 weeks post-cycle: HDL trajectory.
• Symptom diary throughout: Right-upper-quadrant discomfort, jaundice/scleral icterus, dark urine, pruritus, severe fatigue, mood crash — any of these is a stop-and-evaluate signal.