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Bromantane (Ladasten)Small moleculeNo amino acid sequence. Icon reflects category theme only.Also known as: Ladasten, Bromantane, ADK-709
A 728-patient Russian multicenter trial found 90.8% of participants improved on bromantane at 50 to 100 mg daily, with adverse events in just 3%. Bromantane (Ladasten) is a synthetic actoprotector that upregulates dopamine synthesis enzymes rather than flooding synapses like traditional stimulants. No Western clinical trials exist, and WADA bans it outright as a specified stimulant. Biohackers and nootropic users value it for calm, sustained motivation without the crash or jitter that comes with amphetamine-class compounds. Most users cycle 4 weeks on.
A 90.8% improvement rate in 728 patients. That number comes from a Russian multicenter trial [1] testing bromantane at 50 to 100 mg daily over 28 days for neurasthenia. Adverse events hit only 3% of participants. Bromantane (N-(4-bromophenyl)adamantan-2-amine, also sold as Ladasten) sits on an adamantane scaffold, the same carbon cage behind amantadine and memantine. Russia approved it around 2009 for chronic fatigue with cognitive complaints. The compound first hit international radar when athletes at the 1996 Atlanta Olympics tested positive for it. What separates bromantane from stimulants like modafinil or amphetamines is the mechanism. It doesn't block dopamine reuptake. It doesn't dump monoamines into synapses. Instead, it upregulates tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AAAD), the two rate-limiting enzymes in dopamine production. A single dose can double TH expression in the hypothalamus within two hours [2]. The result is a gradual, sustained lift in dopamine synthesis rather than a spike and crash. Community experience across several hundred documented reports on r/nootropics and peptide forums lines up closely with the clinical data. Users consistently describe calm energy, improved task initiation, and better physical stamina. Effects build over the first week; judging bromantane after a single dose misses the point entirely. Western clinical evidence is thin. No FDA-reviewed trials exist. No English-language double-blind placebo-controlled studies have been published. Most pharmacological data traces back to Russian-language journals or preclinical animal work. That gap is real, and it matters for anyone weighing risk.
Bromantane's primary action is indirect genomic upregulation of dopamine biosynthesis. It increases transcription of tyrosine hydroxylase (TH) mRNA and protein in the hypothalamus, striatum, ventral tegmental area, and nucleus accumbens. It also upregulates aromatic L-amino acid decarboxylase (AAAD), the enzyme converting L-DOPA into dopamine. Together, these increases produce more dopamine without the reuptake inhibition or vesicular dumping of traditional stimulants. The timeline matters. TH upregulation appears within 1.5 to 2 hours of a single oral dose. A 2 to 2.5-fold increase in enzyme expression has been recorded in animal models [2]. This genomic mechanism is why effects build over days of consistent dosing. It also accounts for the low abuse potential; there's no immediate dopamine surge, just a steady upward shift in baseline synthesis capacity. On the anxiolytic side, bromantane strengthens GABA-ergic neurotransmission. The exact molecular target hasn't been fully characterized. It doesn't appear to act on GABA-A benzodiazepine binding sites directly. So you get anxiolytic properties without the sedation, cognitive fog, or dependence risk tied to benzodiazepines. Bromantane also increases expression of BDNF and NGF in certain brain regions (animal data). Those neurotrophic effects could contribute to the cognitive improvements reported with longer use, though human confirmation is sparse. Pharmacokinetically, oral bioavailability sits at approximately 42%. Peak plasma hits around 2.75 hours in females, roughly 4 hours in males. The compound is highly lipophilic and distributes into adipose tissue, which is why its primary metabolite (6-beta-hydroxybromantane) shows up in urine for up to two weeks after a single dose.
Approved in Russia for neurasthenia at 50-100 mg/day x 28 days. Large multicenter trial (728 patients) showed 90.8% improvement on CGI-I scale. Mechanism (TH/AAAD upregulation → dopamine synthesis) is well-characterized in preclinical models. No Western RCTs, no FDA-reviewed trials, no English-language double-blind placebo-controlled data.
PMID 21322821: multicenter trial, 728 patients, 50-100 mg/day x 28 days, 90.8% CGI-I improvement, 3% adverse event rate
All clinical evidence from Russian-language publications. No independent replication in Western trials. Long-term safety data (beyond 28-day cycle) absent from controlled data. No dose-ranging RCT comparing 50 mg vs 100 mg outcomes. Zero new PubMed publications 2024-2026.
Positive consensus. Valued for calm, sustained dopaminergic drive without jitteriness. More useful for physical/work output than pure cognition. Effects build over 5-7 days; first-week assessment discouraged.
Both science and community converge on 50-100 mg/day oral dosing. Clinical efficacy matches community reports of improved energy, motivation, and stress tolerance. Community cycling pattern (4 weeks on/off) aligns with clinical trial duration (28 days). No significant divergence in dose or expected benefits.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 25mg | Daily |
| Moderate | 50mg | Daily |
| Aggressive | 100mg | Daily |
Bromantane is oral. No reconstitution, no syringes, no bacteriostatic water. You're working with either pre-made capsules or raw powder. If you're dosing raw powder, a milligram-accurate scale (0.001 g resolution) is non-negotiable. A kitchen scale won't cut it for 25 to 50 mg doses. Weigh each dose individually or pre-weigh a batch into gelatin capsules. Pre-measured capsules from vendors like SwissChems or BehemothLabz eliminate the weighing hassle. Capsule dosing accuracy depends entirely on the vendor's manufacturing process; always check the third-party COA. A small fatty meal before dosing may improve absorption. Bromantane's oral bioavailability is roughly 42% with significant first-pass metabolism. Fat helps lipophilic compounds cross the gut lining. Morning dosing only. The 8 to 12 hour activity window means anything after noon puts your sleep at risk. Start at 25 mg for the first week. Don't judge effects until day 7 at minimum; the TH/AAAD genomic mechanism takes time to ramp. Cycle 4 weeks on, 2 to 4 weeks off. The cycling isn't about tolerance (clinical data shows none) but about lipophilic accumulation in adipose tissue.
Standard cycling is 4 weeks on at 50-100 mg daily, followed by 2-4 weeks off. Some users run shorter 2-week cycles. Due to lipophilic accumulation in adipose tissue, taking breaks is important even though acute tolerance doesn't appear to develop. The Russian clinical trial used a 28-day continuous dosing protocol. Avoid stacking with other dopaminergic compounds during use.
Primary cycling rationale is lipophilic tissue accumulation, not receptor desensitization or hormonal axis suppression. Bromantane distributes extensively into adipose tissue due to high lipophilicity. With daily dosing, tissue levels build throughout a 4-week cycle. Extended continuous use risks progressive accumulation, particularly hepatic, beyond what the 28-day clinical trial safety data covers. Secondary rationale: the 28-day Russian multicenter trial is the only controlled dosing protocol with safety data, so aligning cycle length to that frame keeps users within the known safety envelope. Clinical data shows no acute tolerance development.
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Expected: Improved motivation, sustained energy, reduced stress reactivity. Cognitive benefits secondary to motivational improvement.
Monitor: Track sleep quality: insomnia is the first flag. Consider baseline and end-of-cycle liver enzymes (ALT/AST) given lipophilic hepatic load.
If using pre-made capsules, skip to step 3. For a 50 mg dose with raw powder, the scale should read 0.050 g.
Place the weighed powder into an empty gelatin capsule or dissolve sublingually. Sublingual is reported to have faster onset, but no bioavailability data exists for that route.
Pair with a small meal containing fat (eggs, avocado, nuts) to support absorption.
If tolerated with no insomnia or headache, increase to 50 mg daily.
After 1 to 2 weeks at 50 mg, you can increase to 100 mg daily if more drive is needed. Do not exceed 100 mg without medical supervision.
Some users taper to 50 mg in the final 3 to 4 days, though no clinical data requires a taper.
Effects taper gradually over 3 to 7 days after the last dose due to adipose tissue release.
Storage: powder and tablets are stable at room temperature (15 to 25 degrees C). For long-term storage of bulk powder, refrigerate at 2 to 8 degrees C.
Reference bioavailability (~42%)
Standard administration. Can be taken with or without food; small fatty meal may increase absorption given high lipophilicity. Pre-measured capsules reduce dosing error.
Potentially faster onset; bioavailability difference vs. oral is unknown
Community-reported faster onset when powder is dissolved sublingually. No pharmacokinetic data comparing sublingual to oral for bromantane. Taste is reportedly bitter/chemical. Not recommended over oral without supporting data.
Complementary BDNF upregulation and ACTH-derived cognitive pathway. Semax provides immediate BDNF/focus via intranasal route while bromantane builds dopamine synthesis capacity over days. Mechanistically independent: no pharmacokinetic interaction documented.
Semax 400-600 mcg intranasal AM + Bromantane 50-100 mg oral AM
Anxiolytic balance. Selank modulates GABAergic activity and reduces anxiety without sedation, complementing bromantane's stimulant-adjacent activation. Core component of the "Russian cognitive triad."
Selank 250-500 mcg intranasal + Bromantane 50-100 mg oral
GI protection and systemic neuroprotection. No direct mechanistic synergy with bromantane. Stacked for gut protection given GI side effects at higher bromantane doses, and for general recovery support.
BPC-157 250 mcg AM + PM on standard protocol; bromantane AM
Higher-potency Semax variant. Provides stronger BDNF effect at lower intranasal dose. Preferred by some users in the cognitive triad stack who find standard Semax underwhelming.
NA-Semax 100-200 mcg intranasal + Bromantane 50-100 mg oral
Bromantane increases dopamine synthesis; MAO inhibition prevents dopamine breakdown. Combined effect could produce excessive dopaminergic stimulation: agitation, hyperthermia, cardiovascular stress.
Do not combineAdditive dopamine-enhancing effects. Bromantane upregulates synthesis enzymes; L-DOPA provides direct precursor loading. Monitor for dopamine excess: agitation, insomnia, dyskinesia.
Do not combineCombined stimulant burden overshoots dopaminergic tone. Amphetamines deplete dopamine stores while bromantane increases synthesis: the combination creates unpredictable dopaminergic strain and cardiovascular risk.
Do not combineAdditive dopaminergic stimulation. Bromantane increases synthesis; agonists directly stimulate D2/D3 receptors. Combined effect may cause dysphoria, compulsive behaviors, or cardiovascular strain.
Do not combinePricing updated 2026-04-09
The biggest safety gap with bromantane is the absence of long-term controlled data. The Russian multicenter trial [1] ran for 28 days in 728 patients at 50 to 100 mg daily. Adverse events appeared in roughly 3% of participants. That's a reassuring number, but 28 days tells you nothing about what happens at month three or month six. Insomnia is the most commonly reported side effect, both in clinical data and across community forums. Bromantane's 8 to 12 hour duration of action means afternoon dosing reliably disrupts sleep. This complaint appears dose-independent; even 25 mg taken too late causes problems. The fix is straightforward: dose before 9:00 AM. Headache and tension surface mainly above 100 mg. At standard doses (50 to 100 mg), headaches are occasional and generally resolve with hydration. Users pushing to 150 mg report tension headaches as a consistent limiter. Paradoxical anxiety has been flagged by a subset of community users at doses exceeding 100 mg. The anxiolytic effect inverts in some individuals when dopaminergic tone gets too high. Reducing the dose resolves this. GI discomfort (loose stools, mild nausea) appears at higher doses. Mild dry mouth is reported intermittently. Mydriasis (pupil dilation) occurs at standard doses in some users. It's a marker of dopaminergic activity, not a safety concern, but it can cause photosensitivity. Hepatic strain is a theoretical risk. Bromantane is highly lipophilic and undergoes extensive first-pass hepatic metabolism. It accumulates in adipose tissue throughout a cycle. Liver enzymes (ALT, AST, GGT) should be checked at baseline and at the end of each 4-week cycle, particularly at the 100 mg dose. Any elevation beyond 2x the upper limit of normal warrants stopping. The compound's lipophilicity also means metabolites (primarily 6-beta-hydroxybromantane) remain detectable in urine for up to two weeks after a single dose. Competitive athletes under WADA jurisdiction cannot use bromantane; it's classified as a specified stimulant under category S6. Skin rash is listed in available data but frequency is unclear. Pregnancy and breastfeeding: no reproductive safety data exists. Children under 18 have not been studied. Anyone with severe hepatic impairment, known hypersensitivity to adamantane-class compounds, or active psychotic disorders should avoid bromantane. Stop use and consult a physician if you experience persistent insomnia despite early dosing, skin rash, mood instability, or any signs of liver strain.
Verify Bromantane (Ladasten) dosing and safety with a second opinion
Oral compound sold as unregulated research powder or capsule. No FDA oversight of manufacturing quality, potency, or purity. Mislabeled or underdosed product is the primary risk. Bromantane is not injectable, eliminating contamination/sterility concerns, but powder purity variance affects dosing accuracy. Chinese bulk supply chains dominate the market. Adulteration is a theoretical risk given the price point.
| Test | When | Target |
|---|---|---|
| Liver enzymes (ALT, AST, GGT) | Baseline before first cycle; end of each 4-week cycle | ALT <35 U/L, AST <40 U/L (lab-dependent); increase >2x ULN warrants cessation |
| Sleep quality tracking (diary or wearable) | Daily throughout cycle | — |
| WADA detection window planning | Prior to any in-competition period | — |
Bromantane is highly lipophilic with extensive hepatic metabolism. Accumulation in hepatic tissue creates theoretical hepatotoxicity risk with repeated cycling, particularly at 100 mg/day.
Insomnia is the most common adverse effect and earliest indicator of dosing problems (too late in day, too high a dose). Objective tracking is more reliable than self-report.
Bromantane and its metabolite (6-beta-hydroxybromantane) are detectable in urine for up to 2 weeks after a single dose due to slow adipose release. Athletes must stop at minimum 2 weeks before competition; this is not a guarantee of clearance.
Subtle effects may begin within hours of the first dose as TH upregulation kicks in. Most users report a gentle lift in mood and motivation without obvious stimulation. Some notice reduced background anxiety. Effects are mild as the genomic mechanism is still ramping up.
Dopamine synthesis upregulation reaches meaningful levels with consistent daily dosing. Users typically report improved focus, mental clarity, and a sense of calm drive. Physical stamina may start to improve. The combination of stimulant and anxiolytic effects becomes more apparent.
Peak effects for most users. Sustained improvements in motivation, cognitive stamina, and stress tolerance. Some report improved verbal fluency and task initiation. Physical endurance benefits are more noticeable. BDNF-related neuroplasticity effects may begin contributing.
Final week of a standard cycle. Benefits should be well-established. Begin planning the off-cycle period. Some users taper to 25-50 mg for the last few days rather than stopping abruptly, though there's no clinical data mandating a taper.
Effects taper gradually over 3-7 days due to tissue accumulation. Metabolites remain detectable in urine for up to two weeks. Most users don't report a significant rebound or withdrawal. Maintain any cognitive habits or routines established during the cycle.
Days 1 to 3 (Genomic Priming): TH upregulation starts within 1.5 to 2 hours of the first dose, based on animal data. But meaningful dopamine increases take repeated dosing to build. Most users notice subtle changes at best, maybe a gentle mood lift or reduced background anxiety. Some feel nothing. That's expected, and increasing the dose at this point won't help. Days 4 to 7 (Dopamine Synthesis Ramp): Consistent daily dosing brings TH and AAAD enzyme levels to functional upregulation. This is when the effects click for most people. Improved focus, calm energy, better task initiation. Physical stamina starts climbing. The community consensus is clear: evaluate bromantane here, not in the first three days. Insomnia remains the most common complaint; GI changes are occasionally reported. Weeks 2 to 3 (Peak Effect Window): Full enzyme upregulation is maintained. BDNF and NGF expression may be rising (animal models). The Russian multicenter trial peaked at this timeframe. Users report the strongest motivation, cognitive stamina, and stress tolerance here. Verbal fluency and task follow-through improve. Physical endurance benefits become more obvious. Side effects are minimal at correct dosing and timing. Headache at higher doses and paradoxical anxiety occasionally appear at this stage. Week 4 (Cycle Completion): Benefits hold steady. Lipophilic accumulation in adipose tissue has been building throughout the cycle. Some users drop to 50 mg for the last few days. Begin planning the off-cycle period. No new side effects are expected. Off-Cycle Weeks 1 to 3 (Tissue Clearance): Bromantane releases slowly from fat stores. The primary metabolite (6-beta-hydroxybromantane) stays detectable in urine for up to two weeks. Effects taper over 3 to 7 days, not overnight. Most users don't report rebound or withdrawal. The habits and routines built during the cycle tend to stick.
TH upregulation begins within 1.5-2 hours of first dose (animal data). Dopamine synthesis increases are gradual: enzyme upregulation requires repeated dosing to reach meaningful levels.
Subtle mood lift and reduced background anxiety noted by some. Most report minimal effects. A few notice improved motivation within 24-48 hours.
TH and AAAD enzyme levels reach functional upregulation with consistent daily dosing. Dopamine production meaningfully elevated above baseline.
Improved focus, calm energy, better task initiation. Physical stamina improving. Community consensus: evaluate effects here, not in days 1-3.
Full TH/AAAD upregulation maintained. BDNF and NGF expression potentially elevated (animal models). Russian trial showed peak CGI-I improvement by day 28.
Peak motivation, cognitive stamina, stress tolerance. Improved verbal fluency and task follow-through. Physical endurance benefits more pronounced. Primary benefit window for most users.
Effects well-established. Russian trial endpoint at 28 days. Lipophilic accumulation in adipose tissue is occurring throughout the cycle.
Benefits maintained. Some users taper to 50 mg for the final 3-4 days. Begin planning off-cycle.
Slow release from adipose stores. Primary metabolite (6-beta-hydroxybromantane) detectable in urine for up to 2 weeks post-cessation. Effects taper 3-7 days after last dose.
Gradual return to baseline. No significant rebound or withdrawal. Most users maintain behavioral habits established during cycle.
Source: Reported pharmacokinetic half-life of approximately 11.21 hours for the parent compound. Metabolites (primarily 6-beta-hydroxybromantane) detectable in urine for up to 2 weeks due to slow release from adipose tissue storage. Oral bioavailability ~42%.
Loading the interactive decay curve.
Bromantane is not approved by the FDA for any indication. It has no active IND or NDA on file with any Western regulatory agency. Russia approved it under the brand name Ladasten around 2009 for the treatment of neurasthenia (chronic asthenic conditions). In the United States, bromantane is sold as a research compound. It's not a controlled substance under the Controlled Substances Act, but it has no regulatory pathway for human therapeutic use. Purchasing it as a research chemical is legal in most US states, but it cannot be marketed for human consumption. WADA classifies bromantane as a specified stimulant under category S6 of the Prohibited List. It is banned both in-competition and out-of-competition. Metabolites are detectable in urine for up to two weeks after a single dose. Bromantane is not available through US compounding pharmacies, as it is not an approved compounding ingredient. This content is for educational and research purposes only. It does not constitute medical advice. Consult a licensed healthcare provider before using any research compound.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
