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.
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.
Dihydroboldenone
DHB / 1-Testosterone — 5α-dihydro analog of boldenone (a 1-dehydro DHT). Underground bodybuilding AAS infamous for severe post-injection pain and a tiny formal evidence base.
Aliases (12)
Overview
What is Dihydroboldenone?
Dihydroboldenone (DHB), also known as 1-testosterone, δ1-DHT, or 1-T, is a synthetic anabolic-androgenic steroid — structurally the 5α-dihydro analog of boldenone (Equipoise) and equivalently the 1-dehydro analog of dihydrotestosterone (DHT). Most commonly sold as 1-testosterone cypionate at 100 mg/mL on the gray-market injectable AAS scene. Not FDA approved for any indication. DEA Schedule III (functionally since the 2004 Anabolic Steroid Control Act, with DASCA 2014 closing further loopholes). WADA Prohibited List S1.1a — banned in- and out-of-competition. Almost no formal human clinical literature exists; almost everything written about DHB is community-derived from forum reports and UGL marketing material.
Key Benefits
Community-described 'lean mass without water retention' compound — non-aromatizing means no estrogenic side effects (no E2-driven gyno or bloat), modest cosmetic accrual over 8-12 weeks at 200-400 mg/week, dry / vascular appearance in low-body-fat states. Androgenic strength roughly comparable to testosterone in the only published animal assay (Friedel 2006). Modest anabolic effect with reduced DHT-pathway hair-loss acceleration relative to other DHT-class compounds (because 5α-reductase has already acted on the molecule, so finasteride / dutasteride doesn't help — but the effect is not zero either).
Mechanism of Action
Direct androgen receptor (AR) agonist with high transcriptional potency and selectivity (Friedel 2006). Structurally a 5α-reduced steroid (DHT-class) with a 1,2 double bond in the A-ring that distinguishes it from raw DHT — the 1-dehydro modification appears to confer metabolic stability in muscle tissue (DHT alone is rapidly inactivated by 3α-HSD; DHB resists this). Non-aromatizable to estradiol — no E2 side effects but also no E2-mediated HDL preservation, producing a net-worse lipid profile than aromatizing AAS. Cypionate ester provides ~6-8 day plasma half-life enabling 1-2 weekly injections; PIP is severe and well-documented across the community.
Pharmacokinetics
Research Indications
Structural identity
Dihydroboldenone is 17β-hydroxy-5α-androst-1-en-3-one (parent 1-testosterone; C19H28O2; MW 288.43 g/mol; CAS 65-06-5). The cypionate este…
AR binding and transactivation (Friedel 2006)
The Friedel 2006 paper (Toxicology Letters, [PMID 16621347](https://pubmed.ncbi.nlm.nih.gov/16621347/)) is the only meaningful pharmacolo…
SHBG binding and free-T behavior
DHT-class AAS bind sex hormone-binding globulin (SHBG) with high affinity (Saartok 1984, [PMID 6539197](https://pubmed.ncbi.nlm.nih.gov/6…
Ester pharmacokinetics
- Cypionate (1-test cypionate, "DHB cyp") — by far the most common gray-market form. ~6-8 day half-life. Allows once- or twice-weekly inj…
HPG suppression
DHB produces HPG-axis suppression at any therapeutic dose, comparable to other injectable AAS in the same dose-range. AR feedback at the …
What it doesn't do
- No cognitive enhancement. Not a nootropic. AR signaling in CNS is real but produces no meaningful cognitive benefit at gray-market dose…
Peptide Interactions
Required test base. Non-negotiable for DHB monotherapy avoidance.
Maintains testicular volume / Leydig responsiveness; eases PCT.
Community recommendation given DHB's renal-strain signal. NAC additionally provides hepatic antioxidant support given the Friedel hepatomegaly signal.
Class-level harm reduction for the lipid + CV impact.
Both non-aromatizing potent androgens. Compounded HDL crash, magnified androgenic load, stacked CV + renal load. Among the worst recreational AAS combinations.
Mechanically redundant; DHB *is* the 5α-reduced version of boldenone. Same AR signaling, compounded androgenic load, no clear benefit over running either alo…
Compounded androgenic load (hair, skin, prostate) and lipid impact (HDL crash). DHB is itself DHT-class — adding more DHT-class is redundant for muscle and a…
Hepatotoxicity stacking on top of the Friedel hepatomegaly signal.
Mechanistically unnecessary for DHB itself; only consider if running aromatizing AAS at high doses.
Renal + BP load stacking. Particularly relevant for combat athletes who often use chronic NSAIDs for joint / training pain — given community signal of DHB re…
Additive hepatic load.
Mostly mechanistically neutral. NAC, magnesium, fish oil, vitamin D, creatine — no interaction. Caffeine — neutral but watch BP.
Quality Indicators
Clear oil, no precipitate or crystallization
Properly compounded DHB cypionate in carrier oil (typically grapeseed, MCT, sesame, or cottonseed) should be a clear, viscous, pale-yellow solution. No cloudiness, no particulates, no crystalline deposits. DHB has notable crystallization tendency at higher concentrations — this is a signal of the formulation problem that drives PIP.
Lab-tested COA (HPLC / mass spec)
Reputable UGLs provide HPLC purity + mass-spec identity confirmation. Independent labs (Janoshik, Anabolic Lab) routinely test gray-market AAS. DHB is a relatively niche AAS so counterfeit / mislabeling rates are notable — independent testing is not optional for users who proceed despite the SKIP-AT-20 verdict.
Concentration 150-200+ mg/mL = predictable severe PIP
Higher concentration vials are notorious for crippling post-injection pain. Lower-concentration formulations (50-100 mg/mL) reduce PIP at the cost of higher injection volumes. Some users dilute high-mg vials with sterile carrier oil before drawing the dose. There is no concentration that fully eliminates DHB PIP — only mitigation.
Carrier oil composition matters
Cottonseed oil and high benzyl-alcohol formulations cause more local reaction than grapeseed / MCT / sesame at equivalent concentration. UGL formulations vary widely. PIP is partly compound-intrinsic (DHB itself) and partly formulation-dependent (oil + solvents).
Cloudy oil, precipitate, or visible particles
Cloudiness, visible particles, color inconsistency, or sediment indicate degraded product, contamination, or improperly compounded oil. Do not inject.
Counterfeit / mislabeled product
DHB is sometimes substituted with cheaper testosterone enanthate or boldenone undecylenate at 'DHB' prices on lower-tier UGL markets. Lab testing services flag meaningful counterfeit rates across the gray market for this compound specifically.
What to Expect
- Week 1Tolerability and dose-response.
- Week 2-4Early effect window.
- Week 4-8Peak benefit assessment.
- Week 8+Cycle decision point.
Side Effects & Safety 12
Side Effects
- 1Severe post-injection pain (PIP) — the dominant practical reality. 3-7 days per injection of deep, persistent, often disabling pain at the IM site. Mitigation strategies reduce but never eliminate.
- 2HDL crash — DHT-class lipid impact without E2 protection. Often 30-50% HDL drop within 6-8 weeks at 400 mg/week.
- 3Hematocrit elevation — DHB shares the boldenone-class strong erythropoietic effect (community signal; class-level evidence). Hematocrit can climb toward 54-55% in chronic users → therapeutic phlebotomy threshold.
- 4HPG suppression — testicular atrophy, low endogenous T, low LH/FSH, impaired libido on/post cycle.
- 5BP elevation — fluid + vascular effects. 5-15 mmHg systolic typical at 400 mg/week.
- 6Acne, oily skin, accelerated androgenic alopecia in predisposed users — direct AR effects at scalp / sebaceous tissue. Already 5α-reduced, so finasteride / dutasteride cannot protect.
- 7Increased libido / drive (early cycle) — DHT-class CNS effect.
- 8Modestly elevated ALT/AST — Friedel 2006 documented liver weight elevation in rats; human equivalent at typical doses unclear but bumped LFTs are reported in community bloodwork.
- 9Aggression / irritability / mood changes — class-level finding; magnitude in DHB specifically unverified.
- 10Sleep disruption — partly from BP / HCT elevation, partly from PIP-driven discomfort.
- 11Erectile dysfunction during cycle — paradoxical at supraphysiologic dose due to HPG suppression.
- 12Prostate hypertrophy in older users — DHT-class effect.
When to Stop
- Focal segmental glomerulosclerosis (FSGS) — AAS-class evidence (Herlitz 2010, [PMID 19917783](https://pubmed.ncbi.nlm.nih.gov/19917783/)). 10-bodybuilder cohort with proteinuria + renal insufficiency on biopsy-confirmed FSGS. DHB-specific data does not exist; class-extrapolation supports concern, especially with the boldenone-class renal sonography findings of Kantarci 2018.
- Cardiovascular events — combined hypertension + adverse lipid + polycythemia + LV hypertrophy. Class-level (Baggish 2017, Pope 2014).
- Thromboembolic events (DVT, PE) — driven by polycythemia + altered coagulation balance.
- Persistent post-cycle hypogonadism — Rasmussen 2016 ASIH cohort. The SKIP-AT-20 anchor for under-25 users.
- Injection-site abscess / infection — if sterile technique fails. PIP + infection are difficult to distinguish initially but infection requires emergent care.
- Psychiatric — mania, irritability, depression. Class-level signal.
- Baseline (before starting): Full LFT panel, lipid panel (total chol, LDL, HDL, ApoB, triglycerides, Lp(a)), CBC w/ HCT, total + free testosterone, SHBG, estradiol (sensitive assay), LH, FSH, prolactin, BP, ECG, abdominal US, renal panel (creatinine, eGFR, BUN, urine microalbumin / dipstick, urinalysis), baseline kidney structure on ultrasound if extended use planned, hepatitis B/C serology.
- Week 4: full LFT, lipid panel, CBC, BP, renal panel (creatinine, eGFR, urine microalbumin) — monitor HDL nadir, HCT trajectory, BP, kidney trajectory.
- Week 8: full LFT, lipid panel, CBC, BP, renal panel, hormonal panel — last data point in standard short cycle. Watch for HCT >54%, creatinine elevation, proteinuria.
- Week 12: full panel — end-of-cycle assessment.
- Stop drug if: HCT >54%, creatinine rising >25% from baseline, proteinuria on dipstick, ALT/AST >3x ULN, BP >140/90 sustained, HDL drop >50%, palpable injection-site infection, severe mood / aggression changes.
- Post-cycle: weeks 4 / 12 / 24 post for hormonal recovery + lipid + renal — confirm normalization of HPG axis and lipids. Persistent SCr elevation post-cessation = nephrology referral.
References
Friedel A et al. 2006 — 17β-hydroxy-5α-androst-1-en-3-one (1-testosterone) is a potent androgen with anabolic properties (Toxicology Letters)
the single meaningful pharmacology paper; Hershberger rat assay; equimolar to testosterone propionate; equivalent prostate / seminal vesicle / levator ani growth; significant liver weight increase
View StudyParr MK / Diel 2011 — Endocrine characterization of methyl-1-testosterone (Endocrinology)
companion characterization of M1T; mechanistically informative for DHB's 1-en-DHT-derivative family
View StudyHerlitz LC et al. 2010 — Development of focal segmental glomerulosclerosis after anabolic steroid abuse (J Am Soc Nephrol)
class-level FSGS evidence in AAS-using bodybuilders; empirical anchor for renal-strain concern
View StudyKantarci UH et al. 2018 — Evaluation of anabolic steroid induced renal damage with sonography in bodybuilders (J Sports Med Phys Fitness)
boldenone-undecylenate-containing protocols showed elevated renal volume / cortical thickness / echogenicity; class-extrapolation to DHB
View StudyRasmussen JJ et al. 2016 — Former AAS users with persistent hypogonadism (PLoS One)
empirical anchor for SKIP-AT-20 / persistent ASIH risk
View StudyBaggish AL et al. 2017 — Cardiovascular toxicity of illicit AAS use (Circulation)
cardiac MRI baseline for AAS-class CV harm
View StudyPope HG Jr et al. 2014 — Adverse health consequences of performance-enhancing drugs (Endocrine Reviews)
class review of AAS adverse effects
View StudySaartok T et al. 1984 — Relative binding affinity of AAS at AR + SHBG (Endocrinology)
DHT-class SHBG-displacement / free-T elevation mechanism context
View StudyHartgens F, Kuipers H 2004 — Effects of AAS in athletes (Sports Medicine)
class overview of AAS pharmacology
View StudyKicman AT 2008 — Pharmacology of anabolic steroids (Br J Pharmacol)
mechanism-focused class review
View Study1-Testosterone — Wikipedia
general-audience summary; legal sale until 2005, Schedule III since 2005, Friedel 2006 anabolic-androgenic equivalence finding cited
View StudyDesigner Anabolic Steroid Control Act of 2014 (DASCA) — H.R. 4771, 113th Congress
federal legislation expanding CSA AAS definition; closed loopholes for designer-AAS analogs
View StudyDEA Diversion Control: Anabolic Steroids
Schedule III status, federal regulatory framework
View StudyWADA 2026 Prohibited List
S1.1a confirmation for 1-testosterone / DHB; in- and out-of-competition ban
View StudyDrugBank: 1-Testosterone (DB01481)
drug database entry covering pharmacology, mechanism, regulatory status
View StudyLatest research
- cohortEvaluation of anabolic steroid induced renal damage with sonography in bodybuilders (Kantarci et al., J Sports Med Phys Fitness)22 bodybuilders across three protocol groups. Boldenone undecylenate-containing protocols (group 2) produced significantly elevated renal volume, cortical thickness, and echogenicity vs. lower-dose / testosterone-only groups. BUN and creatinine elevated in high-dose group; urine microalbumin remained normal. DHB is the 5α-reduced analog of boldenone — class-extrapolation supports renal-strain concern.
- cohortCardiovascular toxicity of illicit anabolic-androgenic steroid use (Baggish et al., Circulation)Cardiac MRI cohort of 140 long-term male weightlifters (86 AAS users vs 54 controls). Documented LV systolic dysfunction (lower LVEF) and accelerated coronary atherosclerosis in AAS users; severity tracked cumulative lifetime AAS exposure. Class baseline for AAS-CV harm. DHB-specific data does not exist; this is the extrapolation anchor.
- cohortFormer abusers of anabolic androgenic steroids exhibit decreased testosterone levels and hypogonadal symptoms years after cessation (Rasmussen et al., PLoS One)Case-control study documenting persistent ASIH (anabolic-steroid-induced hypogonadism) >2 years post-cessation. Former users showed lower total/free T, smaller testes, more depressive symptoms, fatigue, ED, and lower libido. Core empirical anchor for SKIP-AT-20 logic — HPG axis maturation is incomplete in late teens / early 20s and exogenous AAS exposure during this window may produce permanent suppression.
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