Methenolone
EmergingMild DHT-derived AAS with a "clean" reputation — non-aromatizing, low androgenic, decent body comp. | AAS · Oil injectable
Aliases (5)
▸ Vial inspection & sterile draw AAS oil
AAS oil arrives pre-suspended in carrier oil — no BAC water needed. Inspect for clarity, color, and crashed compound (cold storage can crystallize). Warm vial in palm or under hot tap before draw.
- 1 Wipe vial stopper with isopropyl alcohol.
- 2 Warm vial 30-60s in palm if oil is cold/cloudy.
- 3 Draw with 18g needle into 22-25g pin barrel for IM, or 27-29g for sub-Q.
- 4 Tap out air bubbles, expel a small drop, then inject at chosen site.
▸ Cycle structure & PCT AAS
Ramp dose over week 1, hold steady through cycle weeks. Track baseline labs (TT/FT/E2/SHBG/HCT/lipids/LFTs) at week 0; recheck at week 4 and end-of-cycle.
On the last dose, the ester clears over its half-life window (enanthate = est. 7 days). PCT begins after the active compound has cleared.
Standard PCT is enclomiphene 12.5-25 mg/day or clomid 50/50/25/25 over 4 weeks (or nolvadex 20/20/10/10). HCG bridge optional during cycle to preserve testicular volume + faster restart. Bloodwork at PCT week 4 + 8 to confirm HPG axis recovery (LH, FSH, TT back to baseline).
▸ Overview TL;DR
Mild DHT-derived AAS with a "clean" reputation — non-aromatizing, low androgenic, decent body comp. SKIP at 20: HPG axis still maturing, suppression risk is real, oral form is hepatotoxic, gray-market product is among the most counterfeited steroids in the world. Cost-per-real-mg often exceeds testosterone by 5-10×.
▸ Mechanism of action
Methenolone is a 1-methylated derivative of dihydrotestosterone (DHT). Two relevant facts flow from this:
- DHT-derived → not a substrate for aromatase, so it cannot convert to estrogen. No gyno risk, no estrogenic water retention, no estradiol-driven HPG feedback (but androgen-driven HPG suppression still happens via central androgen receptor signaling).
- 1-methylation stabilizes the molecule against the 3α-HSD enzyme that normally inactivates DHT in muscle tissue, allowing meaningful AR activity in skeletal muscle (DHT itself is a weak muscle-builder despite being a strong androgen).
Two esters / forms:
- Methenolone enanthate (injectable) — long ester, ~10 day half-life, weekly dosing, NOT C17α-alkylated → low hepatic burden.
- Methenolone acetate (oral) — C17α-alkylated to survive first-pass metabolism → meaningful hepatotoxicity, low oral bioavailability (~30-40%), short half-life requires daily dosing.
Anabolic:androgenic ratio commonly cited as ~88:44-57 (vs testosterone 100:100), meaning roughly half the muscle-building potency of testosterone with reduced (not zero) androgenic side effects. As a DHT-derivative it can still drive androgenic hair pattern issues, prostate effects, and skin effects in susceptible users.
▸ Pharmacokinetics No data
▸Research indications2 use cases
Methenolone enanthate (injectable)
Most effectivelong ester, ~10 day half-life, weekly dosing, NOT C17α-alkylated → low hepatic burden.
Methenolone acetate (oral)
EffectiveC17α-alkylated to survive first-pass metabolism → meaningful hepatotoxicity, low oral bioavailability (~30-40%), short half-life requires…
▸Quality indicators5 checks
▸ What to expect Generic
- 1Week 1-2Frontload phase. Strength gains start; appetite up.
- 2Week 3-4Visible muscle fullness and recovery acceleration.
- 3Week 5-8Peak performance window. Monitor blood pressure + libido.
- 4Post-cyclePCT week 1-4. Bloodwork at week 6 post-cycle.
▸ Side effects + safety
- Common (>10% users):
- HPG axis suppression (always — "mild" suppression is still suppression). LH/FSH drop within weeks.
- Reduced HDL, raised LDL/ApoB (DHT-class lipid impact, less severe than oral 17α-alkylated 19-nors but still meaningful).
- Mild androgenic effects: skin (oily, acne-prone in susceptible users), accelerated androgenic alopecia in genetically predisposed users (DHT-class).
- Less common (1-10%):
- Mood changes (typically mild — irritability, mild aggression).
- Hematocrit elevation (red blood cell mass increase) → cardiovascular risk if untreated.
- Sleep disruption.
- Rare-serious (<1% but worth knowing):
- Oral acetate only: hepatic strain (elevated ALT/AST, cholestasis), peliosis hepatis (rare, dose-and-duration dependent).
- Cardiac remodeling with chronic high-dose use (concentric LV hypertrophy — documented across AAS class, not Primo-specific).
- Persistent post-cycle hypogonadism — documented in young AAS users with otherwise healthy HPG axes, and risk likely higher when HPG axis is still maturing (late teens / early 20s).
- Specific watch periods:
- At age 20: HPG axis is still consolidating final adult set-point. Suppression at this age has higher theoretical risk of permanent change vs same suppression at 30. This is the core SKIP-AT-20 mechanism.
- Liver markers must be checked at week 4 of any oral cycle (acetate form).
▸Interactions3 compounds
- [testosterone-enanthate](testosterone-enanthate.md):SynergisticPrimo is almost always run with a testosterone base in adult cycles — exogenous test prevents the symptomatic crash from suppression of endogenous T while Pr…
- Other DHT-derivatives ([oxandrolone](oxandrolone.md), masteron, winstrol):Avoidstacking multiple DHT-class compounds compounds androgenic side effects (hair, skin, prostate) and lipid impact without proportional muscle-building gain.
- Oral 17α-alkylated AAS together:Avoidliver burden stacks supralinearly.