F

F tier · safety concern

Dihydroboldenone has no human clinical trial data of any kind and its entire dedicated evidence base is a single 2006 rodent and in vitro pharmacology paper, with the term dihydroboldenone not even indexed in PubMed.

dihydroboldenone

ANABOLIC · INJECTABLE ESTER · DHT-DERIVED · NO HUMAN DATA · DEA SCHEDULE III SINCE 2005

also: DHB · 1-testosterone · 1-testosterone cypionate · 5alpha-dihydroboldenone · delta1-dihydrotestosterone · 1-androstenolone

Dihydroboldenone, more properly 1-testosterone, is a 5-alpha-reduced boldenone analogue that was sold legally online in the United States as a prohormone until it was reclassified as a Schedule III controlled substance in 2005. Its entire dedicated scientific literature appears to consist of one 2006 receptor and rodent study, and no human clinical trial of any kind has been published.

the explanation

DHB is a steroid that was sold as a legal supplement in the US until 2005, when it was made a controlled substance. There is essentially one animal study on it and no human research at all, so nothing about its effects or safety in people has actually been measured.

regulatory status

Not approved for any use anywhere; DEA Schedule III since 2005

1-Testosterone was legally sold online in the United States as a prohormone until 2005, when it was reclassified as a Schedule III drug under the Controlled Substances Act. It is named individually in the DEA alphabetical controlled substances table as 17-beta-hydroxy-5-alpha-androst-1-en-3-one under Schedule III. It has never held a medical approval in any jurisdiction and is prohibited in sport.

how it works · proposed mechanism

1-Testosterone is a structurally simple, non-aromatisable androgen receptor agonist whose only characterisation comes from a single preclinical study.

Direct androgen receptor selectivity

The 2006 study found 1-testosterone binds the androgen receptor highly selectively and has high potency to stimulate AR-dependent transactivation. It acts without requiring metabolic activation, which the authors noted characterises it as a typical anabolic steroid.

No aromatisation, no 5-alpha-reduction

Because the molecule is already 5-alpha-reduced and carries a 1,2 double bond rather than a 4,5 one, it cannot be aromatised to oestrogen or amplified further by 5-alpha-reductase. There is no oestrogenic metabolite and no oestrogen-mediated offset to androgen exposure.

Hepatic signal in rodent assay

In the same study, an equimolar dose matched testosterone propionate for prostate, seminal vesicle and levator ani muscle growth but uniquely increased liver weight. That hepatic divergence from the reference androgen has never been followed up in any human study.

together → A single rodent assay showing testosterone-equivalent androgenic potency plus an unexplained hepatic signal is the entire mechanistic foundation, and it has stood without human follow-up for two decades.

what’s reported

0published human clinical trials of dihydroboldenone or 1-testosterone
1dedicated pharmacology study identified (Friedel 2006, in vitro and rodent)
2005year of reclassification to US Schedule III

evidence shape

5 sources

The composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.

official / regulatory2
randomised trials0
observational1
reviews1
preclinical1

⚠ the catch

The name dihydroboldenone is not a PubMed-indexed term at all, and a title search for 1-testosterone returns a small handful of records, almost none of them human. Any specific claim about this compound's effects, potency ratio or safety in people is being made without an underlying human study to support it.

key published findings

  • Preclinical, in vitro and rodent (Friedel 2006, Toxicology Letters): 1-testosterone bound the androgen receptor highly selectively and showed high potency to stimulate AR-dependent transactivation; at an equimolar dose it matched testosterone propionate for stimulating growth of prostate, seminal vesicles and the androgen-sensitive levator ani muscle.
  • Preclinical hepatic signal (Friedel 2006): 1-testosterone treatment uniquely increased liver weight relative to the testosterone propionate reference, a divergence the authors flagged as a health risk warranting regulatory oversight.
  • Bibliometric: a PubMed title search for 1-testosterone returns 17 records and dihydroboldenone is not found in the database at all, with none of the retrieved records being a human clinical trial of the compound.
  • Regulatory (DEA schedules): 1-testosterone is named individually as 17-beta-hydroxy-5-alpha-androst-1-en-3-one under Schedule III, having been reclassified from over-the-counter prohormone status in 2005.
  • Class-level human observational (Baggish 2017, Circulation): 86 long-term AAS users versus 54 non-users showed LVEF 52 ± 11% versus 63 ± 8% and higher coronary plaque volume; no compound-specific data exist for 1-testosterone within such cohorts.

limitations of the evidence

  • There is no human trial, no human pharmacokinetic study and no human safety report specific to this compound, so no evidence-based statement about its effects in people is possible.
  • The single supporting study is a 2006 rodent and cell-based pharmacology paper that has not been replicated or extended in humans in the two decades since.
  • The cypionate ester form marketed for injection has never been formally characterised in any published pharmacokinetic study.

documented safety signals

  • Unexplained hepatic signal: the only dedicated study found 1-testosterone increased liver weight in rodents where the testosterone propionate comparator did not, and the authors explicitly cited associated health risks requiring regulatory oversight; this has never been investigated in humans.
  • No aromatisation means no oestrogen-mediated offset to androgen exposure, removing the bone-protective and lipid-protective oestrogenic signalling that partially buffers testosterone exposure.
  • Expected pronounced androgenic effects on skin, scalp and prostate given the already-5-alpha-reduced structure and demonstrated prostate and seminal vesicle growth in the rodent assay.
  • HPG-axis suppression with reduced LH and FSH, testicular atrophy, impaired spermatogenesis and infertility, expected as an androgen class effect; class data show 27.2% of former AAS users below the lower testosterone reference limit a mean 2.5 years after cessation, with 27.3% reporting erectile dysfunction and 40.1% decreased libido (Rasmussen 2016).
  • Adverse lipid shift with HDL suppression, documented across AAS users (Hartgens 2004: HDL-C 1.08 to 0.43 mmol/l; HDL2-C 0.21 to 0.05 mmol/l).
  • Polycythaemia and raised haematocrit as a general androgen class effect.
  • Cardiomyopathy and accelerated coronary atherosclerosis documented in long-term AAS users generally (Baggish 2017).
  • Total absence of human dose-response data means there is no basis for identifying a threshold at which any of these effects appear, and no contraindication list exists.
  • No approved product exists in any jurisdiction, so identity, purity, sterility and concentration of any circulating material are unverifiable; AAS product-testing data found only 47% of submitted samples contained the labelled substance (HAARLEM).
  • Injection-related infection risk applies to any non-clinical injectable use (Hope 2015: 42% injection-site inflammation, 6.8% abscess or open wound among 366 men injecting image- and performance-enhancing drugs).

identity

full nameDihydroboldenone / 1-testosterone (cypionate ester)
categoryAnabolic & Androgenic
modalitysteroid
formulaC19H28O2
molar mass288.4 g/mol
cas65-06-5

laboratory handling

storageNo approved product and therefore no authoritative storage labelling. General handling of oil-based steroid esters is at controlled room temperature protected from light, but no product-specific stability data have been published for 1-testosterone cypionate.
solubilityPractically insoluble in water. The free steroid is a lipophilic crystalline solid soluble in ethanol and chloroform; the cypionate ester is oil-soluble, though no published formulation or stability characterisation exists.
co-studied withReference note only, not guidance: because no human data exist for this compound in isolation or in combination, any observational harm signal in AAS cohorts that included it cannot be attributed to it, and no interaction profile has ever been studied.

Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.

others in Anabolic & Androgenic

Research use only. dihydroboldenone is catalogued here as a research reagent. Nothing on this page is medical advice, a treatment recommendation, or a dosing protocol. This compound is not for human consumption.