Superdrol
Methasterone · Sdrol · Methyldrostanolone · Methasteron · 2α · 17α-dimethyl-5α-DHT
Last updated
At a glance
400
Testosterone = 100
20
Testosterone = 100
Overview
Superdrol: The Hardest-Hitting Oral in the Playbook#
Superdrol (methasterone) earned its reputation the hard way — as the oral that produces visible, dry, strength-driven gains faster than almost anything else in the AAS toolkit. Structurally it's a 2α,17α-dimethyl DHT derivative, which means no aromatization, no water bloat, and no estrogenic softness. What you get instead is the hard, grainy look of a DHT-family compound stacked with genuinely absurd strength progression — 20–40 lb jumps on the big three inside a month are routinely reported on 10–20 mg/day.
Physique-focused users run it for one of three jobs: a 4-week kickstart to cover the lag on an injectable test cycle, a dry strength block ahead of a meet or peak week, or a recomp push on a TRT base when the goal is "harder and fuller in photos, not heavier on the scale." It is not a cutting compound in the fat-loss sense, and it is not a long-run bulker — it's a short, sharp tool that punches well above its milligram dose.
"10 mg works, 20 mg is the ceiling, 30 mg is where people start posting liver panels." — r/steroids compound consensus
The trade-off is real, and we're not going to soft-pedal it: Superdrol is one of the most hepatotoxic orals in common use, tanks HDL hard, and drives blood pressure up fast. None of that is a dealbreaker for an informed user running it correctly — short cycles, real support compounds, mid-cycle bloodwork, and a proper PCT. The rest of this page covers exactly that: dosing ladders, cycle length, stacking logic, PCT, side effect management, and the specific ancillaries (TUDCA, NAC, telmisartan, tadalafil, taurine, citrulline) that separate a clean Superdrol run from a case report.
How Superdrol works
Superdrol (methasterone) is a 2α,17α-dimethylated derivative of 5α-dihydrotestosterone — structurally, it's Masteron with an added 17α-methyl group for oral bioavailability and a 2α-methyl group that makes it behave very differently in skeletal muscle. Everything that makes it hit hard, and everything that makes it dangerous, traces back to those two methyl groups.
Direct Androgen Receptor Agonism (Without Aromatization)#
Methasterone is a full AR agonist. Because it is already 5α-reduced, it is not a substrate for 5α-reductase, and because its A-ring is saturated it cannot aromatize to estrogen. The practical result is pure androgenic signalling — classical myofibrillar protein synthesis, satellite cell activation, and nitrogen retention — without the estrogenic water retention that inflates the scale on compounds like dianabol. This is why the community calls Superdrol a "dry gainer": the weight that stays is mostly contractile tissue and glycogen, not subcutaneous water.
"Methasterone does not aromatize to estrogen and is a 17α-alkylated oral anabolic steroid, producing 'dry gains' characterized by minimal water retention and significant hepatotoxicity." — Wikipedia contributors, Methasterone, 2024
The 2α-Methyl Group: Why It Hits So Hard#
Muscle tissue inactivates DHT rapidly via 3α-hydroxysteroid dehydrogenase, which is why pure DHT is a terrible anabolic despite binding the AR well. The 2α-methyl substitution sterically blocks this enzyme, letting the molecule linger at the receptor. Combined with the 17α-methyl group (which blocks hepatic first-pass oxidation at C17), the result is an orally active AR agonist that isn't wasted in muscle tissue the way DHT itself is. In the classic rodent bioassays that produced the 400:20 anabolic:androgenic figure, this structural protection is exactly what drove the anabolic uplift.
"These compounds showed increased anabolic activity relative to androgenic effects, with dimethylated derivatives exhibiting an anabolic:androgenic ratio substantially greater than methyltestosterone in standard rodent bioassays." — Arnold A, Potts GO, Beyler AL, Journal of Endocrinology, 1963
Those rodent numbers overstate the human experience — nothing translates 1:1 from a castrated-rat levator ani assay — but they correctly capture the direction: gram for gram, Superdrol is one of the most efficient AR-driven mass builders ever synthesized.
The 17α-Methyl Group: Oral Bioavailability at a Hepatic Price#
The same 17α-methylation that lets the compound survive first-pass metabolism is what drives its hepatotoxicity. 17α-alkylated steroids disrupt bile canalicular transport, producing cholestatic liver injury — bile backs up into hepatocytes, bilirubin climbs, and clinical jaundice often manifests after the cycle has ended rather than during it. This is not a theoretical risk inflated by forum anecdote; it's documented in the peer-reviewed case literature.
"Five young, previously healthy men presented with cholestatic jaundice a median of 2 weeks after discontinuation of methasteron. Peak bilirubin levels ranged from 11 mg/dL to 51 mg/dL and jaundice resolved after 8–12 weeks, with biopsy showing classic features of anabolic steroid-induced liver injury." — Shah NL et al., Clinical Gastroenterology and Hepatology, 2008
The mechanism matters for how you run the compound: TUDCA supports canalicular bile flow, which is the exact pathway under attack, so it's the logical first-line hepatoprotectant. NAC contributes glutathione support against oxidative stress. Neither is a license to run longer — they're triage, not neutralization.
Hepatic Lipase Upregulation and the HDL Crash#
Oral DHT derivatives aggressively upregulate hepatic lipase, which clears HDL particles from circulation. This is why HDL can drop 50–80% within two to three weeks on Superdrol — faster and deeper than almost any other oral. LDL typically rises in parallel, and the full lipid derangement translates to real cardiovascular load: stiffer vasculature, elevated blood pressure, and accelerated atherosclerotic risk if cycles are stacked back-to-back. This is the mechanism behind the "DHT oral lipid wrecking" pattern, and it's why experienced users treat Superdrol as a short, infrequent tool rather than a staple.
Complete HPTA Suppression#
Despite not aromatizing, Superdrol shuts down endogenous LH and FSH production rapidly via direct AR-mediated negative feedback at the hypothalamus and pituitary. Suppression is complete even at 10 mg/day, which is why a proper SERM-based PCT is mandatory on any standalone run, and why the overwhelmingly preferred protocol is to run Superdrol as a 4-week kickstart on top of an injectable testosterone base — the test covers the post-oral recovery window that would otherwise leave the user crashed for weeks.
Read together, the mechanism explains the community consensus perfectly: a potent, non-aromatizing, DHT-derived AR agonist that rewards short cycles and punishes long ones. Respect the structure, respect the 4-week ceiling, and it's one of the most efficient mass and strength tools in the oral category.
Protocol
| Level | Dose | Frequency | Notes |
|---|---|---|---|
| Low | 10–10 mg | Once daily | Documented entry-level range |
| Mid | 10–20 mg | Once daily | Most commonly studied range |
| High | 20–30 mg | Once daily | Once daily works given the 8–12h half-life, but many users split 10mg AM / 10mg PM to flatten peaks and reduce per-dose hepatic burden. Take with food to reduce GI upset. |
Cycle length & outcomes
Documented cycle
2–4 weeks
Plateau after
4 wks
Cycle Length & Structure#
Superdrol is a short-cycle compound, full stop. The hepatotoxicity and lipid damage scale non-linearly past week 4, and there is no version of "more weeks = more gains" that survives a bloodwork review. Run it hard, run it short, get off.
| Goal | Cycle Length | Daily Dose | Structure |
|---|---|---|---|
| First oral cycle (test base) | 3–4 weeks | 10mg | Once daily with food |
| Kickstart to injectable test | 4 weeks | 10–20mg | Weeks 1–4 of a 12-week test cycle |
| Recomp on TRT base | 4 weeks | 10–20mg | Split 10mg AM / 10mg PM |
| Strength peak (experienced) | 3–4 weeks | 20–30mg | Split dosing, tapering into meet week |
| Contest hardening (experienced) | 2–3 weeks | 10–20mg | Final weeks on top of masteron/tren base |
Four weeks is the practical ceiling. Six-week runs exist but are where community case reports of jaundice start showing up.
"'10 mg works, 20 mg is the ceiling, 30 mg is where people start posting liver panels' sums up the community's dosing consensus for Superdrol." — r/steroids community, 2022
Onset & Timing#
Superdrol hits fast. Most users feel strength and fullness changes inside 3–5 days, with visible size and vascularity by the end of week 1. Peak plasma is roughly 1–2 hours post-dose with an 8–12 hour half-life, so once-daily dosing works — but splitting 10mg AM / 10mg PM flattens the peak and reduces per-dose hepatic load. Always take with food.
Strength peaks around week 2–3. Gains plateau by week 4, which happens to coincide with where liver enzymes start climbing aggressively — the compound tells you when to stop.
Loading & Tapering#
No loading. Start at your intended dose from day one. There is no pharmacological benefit to ramping up with an oral AAS of this half-life.
No tapering. Stop abruptly at the end of the cycle. Tapering the dose down doesn't reduce HPTA suppression meaningfully and just prolongs liver exposure. If Superdrol is kickstarting an injectable cycle, you simply drop the oral at week 4 and let the injectable carry the rest.
On-Cycle Bloodwork Cadence#
This is non-negotiable for Superdrol. The damage profile is well-documented and often presents clinically after discontinuation:
"Five young, previously healthy men presented with cholestatic jaundice a median of 2 weeks after discontinuation of methasteron. Peak bilirubin levels ranged from 11 mg/dL to 51 mg/dL and jaundice resolved after 8–12 weeks." — Shah et al., Clin Gastroenterol Hepatol 2008
| Timepoint | Panel |
|---|---|
| Baseline (1–2 weeks pre-cycle) | CMP, lipids, hormones, CBC |
| Mid-cycle (day 14) | CMP (focus on ALT/AST/bilirubin), lipids |
| End of cycle | CMP, lipids |
| 4 weeks post-cycle | CMP, lipids, full hormones (for PCT assessment) |
Monitor blood pressure daily with a home cuff — a 20mmHg systolic rise is routine, and telmisartan 40–80mg or tadalafil 5mg daily should be in place prior to cycle start, not added after you spike.
Bulking vs Cutting#
Bulking: Superdrol shines as a 4-week kickstart to a test-based bulk. Expect 8–15 lb on the scale during the run, with 4–6 lb retained once glycogen and intracellular water normalize. It doesn't aromatize, so the weight you keep is lean — this is the "dry bulk" appeal.
"Methasterone does not aromatize to estrogen and is a 17α-alkylated oral anabolic steroid, producing 'dry gains' characterized by minimal water retention and significant hepatotoxicity." — Wikipedia: Methasterone
Cutting: Superdrol works for contest hardening and recomp but is not a fat-loss compound — it drives nutrient partitioning and visual dryness, not lipolysis. Running it in a steep deficit compounds liver stress (low glycogen, higher bilirubin load) and is the worst-tolerated version of the cycle. If you're cutting, keep calories at or near maintenance during the Superdrol block, then drop calories after you discontinue.
First Cycle Considerations#
Superdrol should not be a true first cycle. A genuine first cycle is test-only at 300–500mg/week for 12 weeks — that's where you learn how your body responds to AAS, calibrate estrogen management, and establish PCT. Using Superdrol as your introduction to AAS stacks a hepatotoxic oral, full HPTA shutdown, and aggressive lipid/BP changes onto a body with no reference point.
When it does enter the picture — typically cycle two or three — start at 10mg/day for 3–4 weeks as a kickstart to a test base. That's the dose that works, and the dose that teaches you the compound without blowing through a liver panel.
Body Transformation Preview
Lean Mass Gain
6.9 lbs
5.2–8.6 lbs range
Fat Loss
0.0 lbs
0.0–0.0 lbs range
Lean Gain by Week
Risks & mistakes
Common (most users)#
- Back and calf pumps — the hallmark Superdrol complaint. Severe enough to cut cardio short or interrupt squat sets. Mitigate with taurine 3–5 g/day, citrulline 6–8 g pre-workout, and aggressive hydration (3–4 L/day). Potassium and magnesium intake matters here too. They don't go away, but they become workable.
- Lethargy and flu-like malaise — usually kicks in around day 10–14. Splitting the dose AM/PM instead of one hit helps. If you're face-down on the couch by week 3, that's the compound telling you week 4 should probably be week 3.
- Appetite suppression — useful on a recomp, annoying on a bulk. Liquid calories (shakes, rice milk, juice + whey) bridge the gap.
- Reduced cardiovascular capacity — expect a visible drop in conditioning. Keep lifting; don't program hard conditioning during the cycle.
- Mild GI upset — take with food. Splitting the dose helps.
- ALT/AST elevation — nearly universal during the cycle. Expected, not dangerous on its own; run TUDCA 500–1000 mg/day and NAC 600–1200 mg/day throughout and for 4 weeks after. Avoid alcohol and acetaminophen entirely.
Uncommon (dose-dependent or individual)#
- Significant blood pressure rise — 20+ mmHg systolic is routine at 20 mg; above 30 mg it scales fast. Check cuff daily. Telmisartan 40–80 mg/day or low-dose tadalafil 5 mg/day manages it. If resting BP crosses 140/90 despite ancillaries, drop the dose or end the cycle.
- Dramatic HDL crash — 50–80% drops are documented for oral DHT derivatives. Pull a lipid panel mid-cycle. Fish oil 3–4 g/day helps marginally; the real mitigation is keeping the cycle at 4 weeks and not stacking orals.
- Acne / oily skin — less than testosterone because it doesn't convert via 5-AR, but susceptible individuals still break out, especially back/shoulders.
- Mood irritability — typical AAS shortening of the fuse. Notice it, manage it.
- Libido swing — often elevated early, can tank late-cycle or during post-cycle transition.
- Prolonged post-cycle crash — HPTA suppression is complete even at 10 mg/day. Running it without a proper SERM PCT (or without an injectable base that pins through the post-cycle window) produces weeks of low-test symptoms.
Mid-cycle bloodwork (CMP + lipids at ~week 2) is not optional at 20+ mg/day. If ALT > 5x ULN or bilirubin rises, end the cycle immediately.
Rare but serious#
- Cholestatic liver injury — the published signature toxicity. Jaundice, dark urine, pale stools, severe pruritus, RUQ pain, vomiting. Classically presents ~2 weeks after discontinuation, not during the cycle.
"Five young, previously healthy men presented with cholestatic jaundice a median of 2 weeks after discontinuation of methasteron. Peak bilirubin levels ranged from 11 mg/dL to 51 mg/dL and jaundice resolved after 8–12 weeks, with biopsy showing classic features of anabolic steroid-induced liver injury." — Shah et al., Clinical Gastroenterology and Hepatology (2008)
- Acute kidney injury — reported alongside severe cholestasis, likely from bilirubin-driven tubular damage rather than direct nephrotoxicity.
"The use of 'Superdrol' (methasteron) was followed by severe painful jaundice, vomiting, and the development of acute renal failure requiring hospitalization, emphasizing the risk of life-threatening toxicity from this oral anabolic steroid." — Nasr & Ahmad, Digestive Diseases and Sciences (2009)
- Pancreatitis — rare, reported in case literature. Severe epigastric pain radiating to the back warrants an ER visit.
- Cardiac remodeling — chronic oral AAS use drives LV hypertrophy and diastolic dysfunction. Not a single-cycle concern, but it's why multiple long Superdrol runs per year is a bad trade.
"17α-alkylated anabolic steroids are well-known for their hepatotoxic effects, particularly canalicular cholestasis, as observed with oral DHT-based agents such as methasterone." — Singh et al., Journal of Clinical and Experimental Hepatology (2023)
Stop immediately if you develop jaundice, dark urine, pale stools, persistent RUQ pain, severe itching, or new epigastric pain. These are not "wait and see" symptoms.
Hard contraindications#
- Pre-existing liver disease (hepatitis, fatty liver with elevated enzymes, Gilbert's with borderline bilirubin, prior DILI) — do not run this compound.
- Untreated hypertension — get BP controlled first, or pick a different compound.
- Pre-existing dyslipidemia — Superdrol will push an already-bad lipid panel into cardiovascular-event territory.
- Concurrent use with any other 17α-alkylated oral (Anadrol, Dbol, Winstrol, Tbol, Halotestin, Anavar) — the hepatic insults stack non-linearly. One oral at a time, full stop.
- Heavy alcohol use, acetaminophen abuse, or any hepatotoxic prescription (methotrexate, isoniazid, high-dose statins, azoles) — same reason.
- Women — virilization risk from a DHT-derived oral is unacceptable at any meaningful dose, and the hepatotoxicity applies equally.
- Pregnancy or potential pregnancy — teratogenic; absolute contraindication.
- Running without a test base past 4 weeks — not a toxicology contraindication but a protocol one: standalone Superdrol past a short run produces a crash that isn't worth the gains.
Gender and PCT considerations#
Women: Superdrol is not a women's compound. Even low doses of DHT-derived orals drive voice deepening, clitoral hypertrophy, and facial hair — changes that are often permanent. There are better tools (Anavar, Primobolan at low dose) for female physique work.
PCT — non-negotiable: HPTA suppression is complete and rapid. On a standalone run, start nolvadex 40/40/20/20 mg beginning 3–4 days after the last Superdrol dose. On a test base, PCT timing is dictated by the injectable's half-life, not the Superdrol — wait for the long ester to clear before starting SERMs. Expect libido, mood, and strength to be down for 4–8 weeks post-cycle even with PCT; pull bloodwork at week 4 post-PCT to confirm recovery. Anyone skipping PCT because "it's just a prohormone" is working from a decade-old playbook that the case-report literature already rewrote.
Stack & combine
Multipliers applied when these compounds run together. Values > 1 indicate a bonus on that axis. Tap a partner to expand the mechanism.
| Partner | Type | Lean | Fat loss | Recovery |
|---|---|---|---|---|
| synergistic | ×1.08 | ×1.00 | ×1.15 |
FAQ — Superdrol
Research & citations
6 studies cited on this page.
Conclusion
Superdrol delivers some of the most dramatic lean mass and strength gains you can get from an oral AAS, but the trade-off in liver and cardiovascular stress is very real — you need to respect it.
Key takeaways:
- Effective starting dose: 10 mg/day; 20 mg/day is an advanced cap — going to 30 mg/day escalates liver risk rapidly
- Typical cycle: 2–4 weeks, never extended past 4; best as a kickstart to an injectable base (test or test/primo)
- Route: oral only; splitting AM/PM helps flatten peaks and reduce per-dose liver load
- Support compounds are not optional: TUDCA 500–1000 mg, NAC, blood pressure meds, fish oil, taurine, and citrulline
- Full SERM-based PCT (nolvadex 40/40/20/20) is required, even for short cycles
- No estrogenic sides, no wet bloat; strength and 'dry', hard muscle gains are rapid
- Hard contraindications: liver disease, untreated hypertension, dyslipidemia, women, stacking with other orals
Run it short, smart, and supported — treat Superdrol with real caution, and you get elite oral results with manageable risk. Abuse it, and you become a case study.