This page describes pharmacological agents that may have legal restrictions, side effects, and drug interactions in your jurisdiction. Information is for educational research only — consult a clinician before considering any compound.

Hepatotoxicity warning

Oxandrolone is 17α-alkylated for oral bioavailability — a structural feature directly responsible for the most severe hepatotoxic class of AAS. Cholestatic injury, peliosis hepatis, and hepatic adenoma are all class-documented. Cycle length must be capped (typically < 6-8 weeks); LFTs (ALT, AST, GGT, bilirubin) baseline + every 2 weeks on cycle. Stop immediately on ALT/AST > 3× ULN or symptomatic jaundice.

High-risk compound

Surface here is educational only; do not use without medical supervision. Our editorial verdict is SKIP-FOR-NOW — current cost / risk / redundancy puts it below the line.

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Oxandrolone

Extensively Studied

Oxandrolone is the canonical "mild" oral anabolic-androgenic steroid — a 17α-alkylated DHT-derivative originally developed by Searle in…

Aliases (8)

Anavar · Oxandrin · Oxandrolone · 17α-methyl-2-oxa-5α-androstan-17β-ol-3-one · BTG-505 · Var · the girl steroid · the mild one

TYPICAL DOSE

HIV wasting: 20mg/day in 2-4 divided doses for …

BID

ROUTE

Oral (tablet)

Oral

CYCLE

6-8 weeks on

Cycle length (4-6 wk)

STORAGE

Room temp; original container

Room temp

Overview

What is Oxandrolone?

Oxandrolone (Anavar) is an oral synthetic anabolic-androgenic steroid (a 17α-alkylated derivative of dihydrotestosterone) FDA-approved as an adjunct therapy for weight gain after surgery, trauma, infection, and chronic illness, and for HIV-associated wasting.

Key Benefits

Promotes lean mass and strength gains with relatively low androgenic and estrogenic side effects compared to other AAS. Used clinically for severe burn recovery, cachexia, and osteoporosis; popular in athletic contexts for "cutting" cycles due to low water retention.

Mechanism of Action

Binds the androgen receptor (AR) in muscle and bone tissue, driving anabolic gene transcription including muscle protein synthesis, IGF-1 expression, and nitrogen retention. The 17α-alkyl group provides oral bioavailability but causes hepatotoxicity.

Pharmacokinetics

PeakHalf-life

Approximate curve — visual aid only, not data-precise PK

▸ Cycle structure & PCT AAS oral

Ester

enanthate

Cycle

6-8 week

Frequency

daily

PCT

Required

Phase 1 — On cycle

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.

Phase 2 — Bridge / cease

On the last dose, the ester clears over its half-life window (enanthate = est. 7 days). PCT begins after the active compound has cleared.

Phase 3 — PCT (post-cycle therapy)

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).

Research Indications

Most Effective

What oxandrolone is, structurally

Oxandrolone is 17α-methyl-2-oxa-5α-androstan-17β-ol-3-one — a synthetic anabolic-androgenic steroid derived from dihydrotestosterone (DHT…

Effective

Receptor + signaling

Oxandrolone is a direct androgen receptor (AR) agonist, with binding affinity comparable to testosterone at peripheral AR (skeletal muscl…

Investigational

Why "non-aromatizable" matters

Most testosterone esters (test enanthate, cypionate, propionate) and methylated derivatives (methyltestosterone, fluoxymesterone) are sub…

Investigational

HPG suppression mechanism even at "mild" doses

Despite the "mild" reputation, oxandrolone produces dose-dependent suppression of the hypothalamic-pituitary-gonadal axis: - AR activatio…

Investigational

Pharmacokinetics

- Oral bioavailability: ~97% (fed) - Half-life: ~9-10 hours - Peak plasma concentration (T-max): ~1 hour - Protein binding: ~94% (largely…

Peptide Interactions

Testosterone esters (enanthate, cypionate):

Synergistic

Standard "test base" cycle adds oxandrolone for cutting / aesthetic enhancement; test prevents the worst HPG crash + libido loss

Trenbolone:

Synergistic

Synergistic for cutting cycles; compounds cardiovascular + neurologic + lipid risks dramatically

Clenbuterol / T3:

Synergistic

Common cutting stack additions; compound cardiovascular load

GH / IGF-1:

Synergistic

Adds anabolic synergy; compounds cancer / cardiomyopathy / hypoglycemia risks (see igf-1.md)

Other 17α-alkylated orals (methyltestosterone, fluoxymesterone, stanozolol, dianabol, anadrol):

Avoid

Compounds hepatotoxicity dramatically; "oral stacking" widely cautioned against

Hepatotoxic medications (acetaminophen at chronic doses, methotrexate, isoniazid):

Avoid

Additive liver burden

Statins:

Avoid

Pharmacologically logical for AAS users with crashing lipids, but adds hepatic burden — careful monitoring required

Insulin / oral hypoglycemics:

Avoid

No direct contraindication but monitor glucose given AAS effects on insulin sensitivity

Quality Indicators

✓

Pharmacy-dispensed, intact packaging

Prescription tablets in original sealed packaging from a licensed pharmacy.

Generic vs branded

Generics are usually fine but bioavailability can vary slightly; track if you switch.

✗

Unbranded blister or counterfeit risk

Counterfeit pharmaceuticals are a known issue; verify pharmacy and lot if buying internationally.

What to Expect

Week 1-2
Subtle initial effects; users often report "nothing happening yet" — distinguishes oxandrolone from harsher orals (Dianabol, Anadrol) which produce immediat…
Week 2-4
Onset of "fuller" muscle appearance with dry / hard / vascular look (no water retention vs. aromatizing AAS); slight strength gains in the gym; modest pump …
Week 4-6
Peak effects — typically 4-8 lb lean mass gain in trained males, noticeable fat reduction (especially with calorie deficit), pronounced vascularity, "harder…
Week 6-8
Tapering of subjective novelty as receptor effects plateau; lipids deteriorating measurably on bloodwork; libido often noticeably lower as endogenous T cras…

Side Effects & Safety

Common (>10% users at bodybuilder doses):
- Atherogenic lipid changes — HDL drops 30-50% within weeks; LDL rises; ApoB rises. The most universally reported objective side effect on bloodwork.
- HPG suppression — testicular atrophy (mild-to-moderate), reduced endogenous testosterone, low LH/FSH; recovery typically 4-12 weeks post-cycle without PCT, faster with PCT
- Hepatotoxicity (transaminitis) — ALT/AST elevation, dose-dependent; typically reversible on cessation; monitor at 4 weeks if running long cycle
- Mild libido changes (initially up, later down as HPG suppression takes hold)
- Skin / hair changes (less than other AAS but not zero) — mild acne, scalp hair shedding in genetically predisposed users
- Forearm / bicep "pumps" — transient, dehydration-related, typical of DHT-derived AAS
Less common (1-10%):
- Cholestatic jaundice — yellowing of skin / sclera, dark urine, pruritus; reversible on cessation
- Mood changes — mild irritability, occasional aggression; less than test or tren but reported
- Sleep disturbance in some users
- Hypertension — modest BP elevation, dose-dependent; less than test
- Erythrocytosis — mild hematocrit increase; less than testosterone esters
- Gynecomastia — RARE on oxandrolone (non-aromatizable) but possible if running with aromatizing AAS or in users with high baseline E2
- Virilization in women — clitoral hypertrophy, voice deepening (may be irreversible), hirsutism, menstrual disruption — main reason women's doses stay <10mg/day
Rare-serious (<1% but worth knowing):
- Peliosis hepatis — cystic blood-filled hepatic lesions; documented case reports with chronic high-dose 17α-alkylated AAS use; potentially life-threatening (hepatic hemorrhage)
- Hepatocellular adenoma / carcinoma — extremely rare but documented with long-term high-dose 17α-alkylated AAS exposure
- Severe atherogenic dyslipidemia leading to accelerated CVD — particularly with cumulative multi-cycle use over years; comparable to other oral AAS profiles
- Cardiomyopathy — extrapolated from broader AAS literature (Baggish et al. cardiac MRI studies of long-term users); cumulative exposure-dependent
- Severe HPG suppression with prolonged hypogonadism post-cycle — secondary hypogonadism failing to recover, requiring TRT salvage; risk rises with cycle length and individual susceptibility
- Mood crash / post-cycle depression — well-documented bodybuilding-community phenomenon; persistent anhedonia / low mood for weeks-to-months post-cycle in susceptible users
Specific watch periods:
- Week 4 of any cycle: ALT/AST + lipid panel — flag if ALT >3× ULN or HDL drops >50%
- End of cycle: Full HPG panel (T, LH, FSH, E2) to confirm degree of suppression
- Week 4-8 post-cycle: HPG recovery check; if still suppressed, formal PCT or endocrinology consult
- Multi-cycle users (years): Periodic echocardiogram, lipid trend tracking, liver imaging if any symptom