Bromantane (Ladasten)
Bromantane (Ladasten) scored 7.1 / 10 (💪 Strong recommend) on the BioHarmony scale as a Substance → Pharmaceutical / Drug → Other Pharmaceutical.
Bromantane is a Russian-developed adamantane actoprotector that scored 76.0% CGI-S responder rate in 728 outpatients (Voznesenskaia 2010, open-label, 50 to 100 mg/day, 28 days). Single-country evidence base and a 2018 Pharmstandard manufacturing exit hold the BioHarmony score at 6.3 / 10.
What is Bromantane (Ladasten)?
Bromantane is a Russian-developed adamantane actoprotector that scored 6.3 / 10 because the Voznesenskaia 2010 trial reported a 76.0% CGI-S responder rate in 728 outpatients with asthenic syndrome but the literature is single-country, single-funder, and the manufacturer let the Russian registration lapse. The drug works by inducing tyrosine hydroxylase gene expression and demethylating the TH promoter (Vakhitova 2006), with downstream BDNF and NGF mRNA upregulation (Salimgareeva 2012). It is on the WADA Prohibited List for sport since 1997 and is not FDA-approved.
Bromantane, also marketed in Russia as Ladasten and known by the laboratory designation ADK-709 or N-(4-bromophenyl)-2-adamantylamine, is the prototype compound of an unfamiliar drug class: the actoprotector. Actoprotectors increase physical and intellectual performance under stress without increasing oxygen consumption or heat production, which is the pharmacological feature that distinguishes them from classical stimulants like amphetamines, methylphenidate, or modafinil. The class was developed during the late Soviet era at the V.V. Zakusov State Institute of Pharmacology in Moscow, and Bromantane is the most studied member.
The mechanism is unusual. Original work in 1995 framed Bromantane as a weak monoamine reuptake inhibitor at micromolar concentrations (Kudrin 1995), but in-vivo therapeutic concentrations are well below those numbers, so the reuptake-inhibition model does not explain the clinical picture. The current mechanistic consensus, established by the Vakhitova / Seredenin / Mikhaylova group, is that Bromantane acts upstream by activating dopamine biosynthesis. A single 50 mg/kg dose in rats induces tyrosine hydroxylase and DOPA-decarboxylase gene expression (Vakhitova 2004), produces cytosine demethylation in CpG islands of the TH gene promoter in hypothalamic cells (Vakhitova 2006), and increases BDNF and NGF mRNA in striatum, hypothalamus, and hippocampus with pERK1/2 up 70% at 30 minutes (Salimgareeva 2012). The most rigorous paper, Mikhaylova/Behnisch 2007 in Neuropharmacology, showed that hippocampal short-term potentiation converts to long-lasting LTP under Bromantane in a manner reversible by the D1 antagonist SCH23390. This is the only Western-journal mechanism paper for Bromantane.
The clinical case is narrower. The compound is approved in Russia for asthenic disorders and was the indication of one large open-label multicenter trial in 728 outpatients (Voznesenskaia 2010, CGI-I responder 90.8% at 50 to 100 mg/day for 28 days, with benefit persisting at least one month post-discontinuation) and one published placebo-controlled RCT (Neznamov 2009, 28 days, no withdrawal syndrome). There are zero Western RCTs, zero Cochrane reviews, zero NIH-funded studies, and zero ClinicalTrials.gov registrations as of May 2026. Pharmstandard discontinued the Russian Ladasten brand in 2018 and the registration lapsed, while Algernon Pharmaceuticals retired the NP-160 program after announcing positive but never-peer-reviewed 2019 NASH and CKD preclinical data. Two industrial actors walked away from Bromantane, which is a meaningful evidence-integrity signal.
Terminology
Bromantane sits at the intersection of three disciplines, each of which uses different terminology, so a quick glossary clarifies the mechanism and trial discussion below. Most readers will already recognize half of these from other nootropic reading; the rest are specific to the actoprotector class or the asthenia clinical literature.
- Actoprotector: A drug class that increases physical and intellectual performance under stress without increasing oxygen consumption or heat production. Distinct from classical stimulants. Developed in the late Soviet era.
- TH (Tyrosine Hydroxylase): The rate-limiting enzyme in dopamine biosynthesis. Bromantane upregulates TH gene expression rather than blocking dopamine reuptake.
- DAT, SERT, NET: Dopamine, serotonin, and norepinephrine reuptake transporters. Bromantane has weak in-vitro affinity at all three at micromolar (not nanomolar) concentrations.
- BDNF / NGF: Brain-Derived Neurotrophic Factor and Nerve Growth Factor. Both are induced at the mRNA level by Bromantane in striatum, hypothalamus, and hippocampus.
- CGI-S / CGI-I: Clinical Global Impression - Severity and Improvement. Standard psychiatric outcome scales used in the Voznesenskaia 2010 multicenter trial.
- Asthenia / Neurasthenia: ICD-10 diagnostic category F48.0 covering chronic mental and physical fatigue with autonomic and emotional features. The Russian regulatory indication for Bromantane.
- WADA S6.A: World Anti-Doping Agency Prohibited List, Section 6 Stimulants, Subsection A (non-specified stimulants). Bromantane has been listed since 1997.
- EIA (Evidence Integrity Adjustment): A penalty applied within the BioHarmony scoring methodology when industry funding combines with manufacturer or developer withdrawal, or with failed independent replication. Bromantane carries a 1.0-point downward adjustment.
- Ladasten: The Russian brand name marketed by Pharmstandard. Manufacturing was discontinued in 2018, and the registration lapsed.
How do you take Bromantane (Ladasten)?
Dosing & Protocols
Dosing information is summarized from published research and community reports. This is not a prescribing guide. Consult a healthcare provider before starting any protocol.
View 1 route and 3 protocols
Routes & Forms
| Route | Form | Clinical Range | Community Range |
|---|---|---|---|
| Oral | Capsule or tablet, 50 mg or 100 mg (Russian Ladasten brand) or research-chemical bulk powder | 50 to 100 mg/day for 28 days Russian Phase III asthenia trial (PMID 21322821) used 50 to 100 mg/day for 28 days. | 30 to 200 mg/day Nootropic-community reports cluster at 50 to 100 mg single morning dose. Some users report a strong response at 30 mg with a different effect profile at 100 mg. Dosing past 200 mg trends toward agitation and dysphoria in forum reports. |
Protocols
Low-dose pulse (Nick's protocol) Anecdotal
- Dose
- 30 mg
- Frequency
- As needed, morning only, not daily
- Duration
- Pulsed when an actoprotector lift is wanted; cycled rather than continuous
30 mg gets the actoprotector profile cleanly; the effect signature shifts toward more dopaminergic prominence at 100 mg, which most users do not need. Non-daily and pulsed dosing avoids the tolerance and theoretical downregulation concerns that come with chronic use, and aligns with the absence of long-term human safety data.
Russian clinical (asthenia) Clinical
- Dose
- 50 to 100 mg
- Frequency
- Once daily, morning
- Duration
- 28 days
Used in the n=728 multicenter trial ([Voznesenskaia 2010](https://pubmed.ncbi.nlm.nih.gov/21322821/)). Therapeutic benefit persisted at least one month after the course ended. This is the registered Russian asthenia protocol, not a recommendation for routine personal use.
Community 4-on / 4-off cycle Anecdotal
- Dose
- 50 to 100 mg
- Frequency
- Once daily, morning
- Duration
- 4 weeks on, 4 to 8 weeks off
No published cycling RCT. Rationale combines the 28-day trial duration, the 1-month carryover, and the absence of long-term safety data.
How this score is calculated →
What are the benefits of Bromantane (Ladasten)?
Upside contribution: 2.54
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Efficacy | 25% | 3.8 | 0.950 | |
| Breadth | 15% | 3.0 | 0.450 | |
| Evidence | 25% | 3.3 | 0.825 | |
| Speed | 10% | 4.0 | 0.400 | |
| Durability | 10% | 3.9 | 0.390 | |
| Bioindividuality | 15% | 3.5 | 0.525 | |
| Total | 3.540 |
Upside Rationale
Bromantane delivers a genuinely useful upside because it rebuilds depleted dopaminergic drive rather than borrowing against it. The strongest signal is in asthenia, where a 728-patient outpatient cohort logged a 76.0% CGI-S responder rate at 50 to 100 mg/day over 28 days, with benefit carrying past the dosing window (Voznesenskaia 2010). That magnitude was then anchored by a placebo-controlled trial confirming superiority over placebo on asthenia load (Neznamov 2009). What makes Bromantane unusual is the dual profile: a stimulant-shaped response in some users and an anxiolytic-shaped one in others (Neznamov 2008), so a meaningful subset gets energy without the jitter typical of dopaminergics. Real clinical magnitude, not a marginal nudge.
Bromantane offers moderate breadth, clustered tightly around one mechanism rather than sprawling across unrelated body systems. The fatigue and asthenia axis is the load-bearing claim, with human trial support on both ends (Voznesenskaia 2010, Neznamov 2009). Around that core sit stress-resilience effects, with animal models showing protection against heat, hypoxia, and combined stressors (Morozov 1999), and a cognition arm supported mechanistically through D1- and D5-dependent hippocampal plasticity (Mikhaylova 2007). The breadth is real but bounded: Bromantane does not reach into cardiovascular, metabolic, or longevity territory, so it earns a mid-band score for doing a related family of things well rather than everything thinly.
Bromantane rests on a credible clinical record for a compound this far outside Western pharma. The base is one large multicenter trial plus a placebo-controlled RCT, backed by roughly thirty mechanistic preclinical papers (Voznesenskaia 2010, Neznamov 2009, Morozov 1998). That earns Bromantane real evidentiary credit: a consistent Russian clinical and actoprotector record showing the same recovery phenotype across human and animal work, with no penalty for the simple absence of a Western RCT. The score stays mid-band rather than high because the body of work concentrates in a single national research tradition and the original developer let the registration lapse. The data that exists is coherent and points the same direction; it is just geographically narrow.
Bromantane acts fast enough to feel within the first few days, which is quick for a mechanism built on gene induction. The Russian label cites a therapeutic effect inside 1 to 3 days, and subjective stimulation typically begins within a couple of hours of an oral dose given a Tmax near 3 to 4 hours and a half-life around 11 hours (Oliynyk and Oh 2012). Full asthenic relief consolidated over the first 1 to 2 weeks in the clinical cohort, which logged readings at days 3, 7, 14, and 28 (Voznesenskaia 2010). That is slower than a same-day stimulant but markedly faster than antidepressants. For a compound that works by upregulating dopamine biosynthesis, a multi-day onset is the expected and favorable signature.
Bromantane holds its gains unusually well, because the benefit comes from a recovery phenotype rather than transient receptor occupancy. Therapeutic improvement persisted at least one month after the drug was stopped in the clinical cohort, which is atypical for a stimulant and fits a mechanism that outlasts plasma exposure (Voznesenskaia 2010). A two-month rodent course showed no tolerance buildup and a clean return to baseline afterward (Iezhitsa 2000). The durability is strong without tipping into permanence, which is the desirable middle: effects that compound over a cycle and then wash out cleanly, supporting the standard four-weeks-on, four-to-eight-weeks-off rhythm rather than open-ended daily use. No long-run cycling trial exists to extend the claim further.
Bromantane responds well to individual tuning, which is a feature rather than a liability for an experienced user. The same dose produces different drug profiles depending on baseline cortical state, shifting stimulant-shaped in some users and anxiolytic-shaped in others (Neznamov 2008), and pharmacokinetics differ by sex in Tmax and half-life (Oliynyk and Oh 2012). A meaningful low-dose responder cohort exists, with the effect character changing between roughly 30 mg and 100 mg, so dose itself becomes a lever for whether Bromantane reads as activating or calming. Some dopaminergic-sensitivity variance shows up as occasional agitation or insomnia, which is why titration matters. The upshot for Bromantane is high personalizability: response is consistent enough to be reliable yet tunable enough to dial in.
What are the risks & downsides of Bromantane (Ladasten)?
Downside contribution: 0.89 (safety risks weighted extra)
| Dimension | Weight | Score | Visual | Weighted |
|---|---|---|---|---|
| Safety | 30% | 1.8 | 0.540 | |
| Side effects | 15% | 1.7 | 0.255 | |
| Cost | 5% | 2.5 | 0.125 | |
| Effort | 5% | 1.9 | 0.095 | |
| Opportunity | 5% | 1.6 | 0.080 | |
| Dependency | 15% | 1.4 | 0.210 | |
| Reversibility | 25% | 1.5 | 0.375 | |
| Total | 1.680 | |||
| Harm subtotal × 1.4 | 1.932 | |||
| Opportunity subtotal × 1.0 | 0.300 | |||
| Combined downside | 2.232 | |||
| Baseline offset (constant) | −1.340 | |||
| Effective downside penalty | 0.892 |
Downside Rationale
Bromantane carries a genuinely benign safety profile, with no intrinsic catastrophic risk on the published record. The large multicenter cohort of 728 patients reported roughly a 3% adverse-event rate, under 1% discontinuation, and zero serious adverse events over 28 days (Voznesenskaia 2010), with no anaphylaxis, organ failure, cardiac, or cutaneous catastrophic signal anywhere in the trial literature. Animal toxicology shows a wide therapeutic margin, with stimulation at moderate doses and full recovery after a two-month course (Iezhitsa 2000). The honest caveats on Bromantane are extrinsic to the molecule: human safety data stops at 28 days, and the original manufacturer let the registration lapse in 2018 (Pharmstandard), pushing supply toward channels with uneven purity. The compound itself is clean; the surrounding data depth and supply chain are the limits.
Bromantane produces mild, infrequent side effects rather than a burdensome profile. At the trial dose of 50 to 100 mg/day, the cohort logged about a 3% adverse-event rate with discontinuation under 1% and zero serious events (Voznesenskaia 2010). The most common reports are mild gastrointestinal upset, transient headache, and occasional insomnia or restlessness in dopamine-sensitive individuals. Under a low-dose cycled protocol the burden is thinner still, because the roughly 11-hour half-life and biosynthesis mechanism do not accumulate on intermittent dosing. The genuine variability around Bromantane comes from sourcing, not the molecule: gray-market powders can be mislabeled or off-target on content, and one illicit sample was assayed at 33.2 mg per unit in forensic surveillance (Vanhee 2025), so a certificate of analysis on the actual lot is the main mitigation.
Bromantane sits in a low-to-moderate cost band, cheap per dose but with no clean commercial channel. The original Russian brand ran roughly $30 to $50 per month at retail, but that product is no longer manufactured after the 2018 discontinuation. In practice, Bromantane is now bought as bulk research-chemical powder, typically $40 to $100 per gram, which works out to one to three months of clinical-dose supply and a low effective per-dose cost. The financial penalty on Bromantane is modest and offset by a non-monetary tax: the absence of a legitimate Western source means the real spend includes due-diligence effort on vendor quality and third-party assay, not just the sticker price. Cheap molecule, awkward marketplace.
Bromantane asks almost nothing in day-to-day effort. The regimen is a single oral dose, with no titration ladder, no refrigeration, and no special timing beyond taking it in the morning to avoid sleep disruption. The only added complexity is the cycling discipline, a four-weeks-on, four-to-eight-weeks-off rhythm, which is a calendar reminder rather than a real chore. The one upfront effort cost on Bromantane is sourcing: because there is no retail channel, the initial work of vetting a vendor and confirming a certificate of analysis is real, but it is a one-time setup rather than an ongoing burden. Once a trusted lot is in hand, the maintenance effort is among the lowest of any actoprotector.
Bromantane imposes little opportunity cost and stacks cleanly with most adjacent tools. It combines with Selank, Semax, L-tyrosine, and common racetams without obvious interaction, so choosing Bromantane rarely forecloses other options. The modest opportunity cost on Bromantane lives in two narrow places: part of the asthenia or fatigue indication can also be addressed by sleep correction or by Modafinil, which carries FDA approval and a stronger Western evidence base, and the sourcing diligence is time that could go elsewhere. Caution is warranted when layering Bromantane with other dopaminergics. On balance these are minor trade-offs, which is why Bromantane scores low on foregone alternatives.
Bromantane shows no addiction or withdrawal signal, which is its strongest safety distinction. The placebo-controlled trial explicitly characterized Bromantane as producing no withdrawal syndrome and no addictive potential after a 28-day course plus a one-week washout (Neznamov 2009), and no addiction case reports exist in the literature. Unlike classical stimulants, Bromantane works by upregulating dopamine biosynthesis rather than forcing acute release, so the compulsive-use loop that drives dependency does not engage. The only open question on Bromantane is theoretical dopamine downregulation under chronic daily use, which is mechanistically plausible but unstudied and is precisely what the standard cycling protocol is designed to prevent. For practical purposes, Bromantane belongs in the no-dependency-concern category.
Bromantane reverses cleanly when stopped, with no lingering liability. Plasma clearance is essentially complete within about two days given the roughly 11-hour half-life, and the two-month rodent course returned fully to baseline after discontinuation (Iezhitsa 2000). The one nuance is that Bromantane works through gene-expression changes such as TH demethylation, which are mechanistically more durable than plasma levels, and the clinical record does show benefit carrying about a month past the last dose (Voznesenskaia 2010). That carryover is a feature, not a trap: it reverts on its own timeline with no rebound or dependency. Stopping Bromantane is a clean exit rather than a managed taper, which keeps its reversibility firmly in the low-risk band.
Is Bromantane (Ladasten) worth it?
The practical verdict on Bromantane is that it is a reasonable adjunct for asthenic recovery and stress resilience in someone willing to accept gray-market sourcing, willing to use the compound intermittently rather than continuously (Nick's protocol is 30 mg morning, pulsed not daily), and not subject to any sport drug-testing regime. The score lands at 7.1 / 10 (Worth Trying) because the Voznesenskaia 2010 trial signal is strong but the literature is single-country, single-funder, and the manufacturer let the only registered brand lapse. Bromantane scores above Modafinil (5.8) on the strength of its native asthenia signal but below Selank (6.5) and Semax (6.8) on registration durability, and below Ashwagandha (7.0) on breadth. It is meaningfully different from a classical stimulant; the manufacturer-walkaway pattern is what holds it back from the strong-recommend tier.
✅ Best for: Knowledge workers and high-output executives running 30 mg pulsed in the morning (not daily) who want an actoprotector that does not feel like coffee or a classical stimulant; biohackers comfortable sourcing from research-chemical vendors with an HPLC certificate of analysis and willing to use the compound intermittently rather than continuously; users with low-baseline-alpha EEG patterns or post-burnout phenotype who tend to fall in the dual-mechanism responder cohort; people who have tried Modafinil and dislike the wakefulness-without-recovery feel; readers who want a peptide-adjacent stack with Selank or Semax and are aware that the long-term safety record is short.
❌ Avoid if: You are pregnant, lactating, under 18, on an MAOI, or competing in any tested sport (WADA Prohibited List S6.A since 1997, Burnat 1997, Docherty 2008); you have bipolar I, uncontrolled hypertension, or a history of stimulant-induced agitation; you stack high-dose dopaminergics (Modafinil, methylphenidate, amphetamines, L-DOPA, selegiline) without a careful interaction review; you are unwilling to source from a research-chemical vendor and not located in Russia where the brand is no longer manufactured; you want a Western RCT-backed intervention rather than a single-country evidence base; you are sensitive to dopaminergic agitation or insomnia and unwilling to dose only in the morning. Counterfeit and underdosed product is documented in 2025 European forensic surveillance (Vanhee 2025), so gray-market sourcing without HPLC verification is itself a contraindication.
Sourcing & dosing caveat: gray-market supply; score assumes clean, correctly-dosed material.
What is Bromantane (Ladasten) best for?
The overall BioHarmony score reflects the intervention's primary evidence profile. These subratings are independent assessments per use case.
Cognition / Focus: 5.8/10
Score: 5.8/10Cognition support is biologically plausible but lacks a dedicated cognitive-battery RCT. The Voznesenskaia 2010 multicenter trial captured concentration and attention improvement inside the asthenia outcome rather than as a primary endpoint. The Neznamov 2008 EEG study documented a psychostimulant-shaped EEG with alpha-frequency increase in high-baseline-alpha responders. Mechanism support is strongest from Mikhaylova/Behnisch 2007, which showed D1- and D5-dependent conversion of hippocampal short-term potentiation into long-lasting LTP, the paper most often used to anchor cognitive claims. No standalone Stroop, n-back, or RAVLT data, which keeps this score in the worth-trying band rather than top-tier.
Stress / Resilience: 6.0/10
Score: 6.0/10Stress resilience is the defining pharmacology of the actoprotector class. Animal studies document protection against heat, hypoxia, carbon monoxide, and combined stressors with effects 1.3 to 1.6 times phenamine and lasting more than 24 hours after a single dose (Morozov 1998, Oliynyk and Oh 2012). Soviet and Russian operational deployment in military and aerospace contexts is referenced but not RCT-grade (Morozov 1999, Viatleva 2000). Tallerova 2011 showed Bromantane was more potent than imipramine at lowering TNF-alpha and IL-6 in a mouse depression-like inflammation model. Strong mechanistic story; thin human-trial confirmation.
Energy / Fatigue: 6.2/10
Score: 6.2/10Fatigue and asthenia are the best-supported clinical use case for Bromantane. The Voznesenskaia 2010 multicenter trial in 728 outpatients with asthenic syndrome reported a CGI-I responder rate of 90.8% at 50 to 100 mg/day for 28 days, with therapeutic benefit persisting at least one month post-discontinuation. The placebo-controlled Neznamov 2009 trial confirmed superiority over placebo on asthenia symptom load. Mechanistically, TH gene induction plus BDNF/NGF mRNA upregulation supports a sustainable energy-recovery phenotype rather than a stimulant-crash profile (Salimgareeva 2012). Open-label design and single-country evidence base hold this score below the strong-recommend tier.
Anxiety: 5.7/10
Score: 5.7/10Bromantane carries an explicit anxiolytic limb confirmed in the only placebo-controlled human RCT, where Neznamov 2009 characterized the drug as combining psychostimulant and anxiolytic actions in neurasthenia patients. The Voznesenskaia 2010 multicenter cohort reported autonomic stabilization and anxiolytic effects alongside the asthenia outcome. EEG-stratified responder analysis showed an anxiolytic-shaped pattern in low-baseline-alpha patients (Neznamov 2008). Numerical HAM-A or MFI-20 deltas are not abstract-accessible, which is the main reason this lands at the lower edge of Worth Trying.
Mood / Emotional Regulation: 5.5/10
Score: 5.5/10Mood support is moderate and indirect. Voznesenskaia 2010 reported quality-of-life improvements rather than formal mood-scale deltas in the n=728 cohort. The strongest depression-relevant data is animal-only: Tallerova 2011 outperformed imipramine on TNF-alpha and IL-6 in an LPS depression-like model, and Tallerova 2014 reversed social-defeat behavioral despair while normalizing T-cell subsets. Bromantane is not registered as an antidepressant in any jurisdiction, and no human depression RCT exists, which holds the mood score at the Neutral threshold.
| Use Case | Score | Summary |
|---|---|---|
| ○ Depression Primary | 3.5 | Bromantane is not approved or studied as an antidepressant in humans. The depression evidence base is animal-model only (Tallerova 2011, Tallerova 2014) and should not anchor a clinical depression claim. |
| ○ Neuroplasticity | 4.5 | Mechanistic support is reasonable. Hippocampal D1/D5-dependent LTP transformation (Mikhaylova/Behnisch 2007) and BDNF + NGF mRNA induction in striatum, hypothalamus, and hippocampus (Salimgareeva 2012) point to a plasticity-supporting profile. No human imaging or learning-task data. |
| ○ Flow State / Peak Mental Performance | 4.2 | Indirect support via the cognition + drive limb of the EEG responder data, but no flow-state-specific data exists. |
| ○ Sleep Quality | 4.0 | Sleep-wake normalization was reported in Voznesenskaia 2010 as part of the asthenia outcome. Long half-life means PM dosing can compress sleep latency; community reports flag insomnia as the most common subjective AE. |
| ○ Recovery / Repair | 4.0 | The actoprotector pharmacology accelerates restoration after physical and psychological exertion in animal stress-protection paradigms (Oliynyk and Oh 2012), but human recovery RCTs are absent. |
| ○ Memory | 3.5 | Hippocampal LTP support from Mikhaylova/Behnisch 2007 (PMID 17854844) is suggestive but no human memory-battery RCT exists. |
| ○ Endurance / Cardio | 3.5 | Animal data on physical work capacity (Morozov 1998) is consistent but human RCT data is absent. WADA ban makes this category academic for any tested athlete. |
| ○ Creativity / Divergent Thinking | 3.0 | No human creativity data. Mechanism could plausibly support divergent thinking via dopaminergic tone but this is speculative. |
| ○ Immune Function | 3.0 | T-cell subset normalization reported in C57BL/6 stress-anxiety models (Tallerova 2014), but no human immune endpoint. |
| ○ Anti-Inflammatory | 3.0 | TNF-alpha and IL-6 reductions in mouse LPS-depression model (Tallerova 2011) and IL-6, IL-17, IL-4 reductions in C57BL/6 anxious-depression model (Tallerova 2011 EKF). No human inflammation RCT. |
| ○ Libido / Sexual Health | 3.0 | Animal data: Khamidova 2005 showed restoration of stress-impaired spermatogenesis and fertilizing capacity in male rats (PMID 16047676) and Kuzubova 2004 reported dose-dependent proceptivity and receptivity changes (PMID 15341065). No human libido RCT. |
| ○ Fertility (Male) | 3.0 | Khamidova 2005 rat reproduction study showed restoration of stress-violated spermatogenesis (PMID 16047676). Animal-only signal; not a human fertility intervention. |
| ○ Substance Use / Addiction Support | 3.0 | Often discussed in the context of the dopamine-biosynthesis mechanism for post-substance fatigue and apathy, but no published human addiction-recovery RCT for Bromantane exists. Treat as speculative. |
| ○ Neuroprotection | 3.0 | BDNF and NGF mRNA induction (Salimgareeva 2012) is plausible neuroprotection support, but no neuroprotection RCT or biomarker data exists. |
Frequently Asked Questions
What does Bromantane actually do?
Bromantane is an indirect dopaminergic actoprotector that increases dopamine synthesis through tyrosine hydroxylase gene induction rather than blocking reuptake. The strongest mechanistic evidence is Vakhitova 2006, which documented cytosine demethylation of the TH promoter in rat hypothalamus, and Mikhaylova/Behnisch 2007, the only Western-journal paper, which showed D1- and D5-dependent conversion of hippocampal short-term potentiation into long-lasting LTP. Salimgareeva 2012 added BDNF and NGF mRNA induction with pERK1/2 up 70% at 30 minutes.
How much Bromantane should I take, and when?
Most users do well with 30 mg taken in the morning, pulsed rather than daily, which gets the actoprotector profile cleanly without unnecessary dopaminergic load. The Russian Phase III asthenia indication used 50 to 100 mg/day for 28 days (Voznesenskaia 2010), but the registered clinical protocol is for asthenic disorders and is not what most readers are dosing for. The effect signature shifts at 100 mg toward more dopaminergic prominence. Avoid afternoon and evening dosing because the half-life is roughly 11.2 hours. Cycle rather than dose continuously: there is no long-term human safety data past 28 days.
What does the human evidence actually show for Bromantane?
The evidence base is one open-label multicenter trial of 728 outpatients (CGI-S responder 76.0%, CGI-I responder 90.8%, Voznesenskaia 2010) plus one published placebo-controlled RCT (Neznamov 2009) where sample size and effect sizes are not in the abstract. There are zero Western RCTs, zero Cochrane reviews, zero NIH-funded studies, and zero ClinicalTrials.gov registrations as of May 2026. The closest Western touchpoint is the Oliynyk and Oh 2012 narrative review.
Is Bromantane safe long-term?
Long-term human safety data does not exist. The largest published trial ran 28 days (Voznesenskaia 2010, AE rate 3%, discontinuation 0.8%, no SAEs in n=728), and the only placebo-controlled RCT was 28 days plus a one-week washout (Neznamov 2009, no withdrawal syndrome). Bromantane is not FDA-approved and there is no FAERS surveillance data. The closest analog is a 2-month rat course showing recovery within 2 months and no tolerance (Iezhitsa 2000). Pharmstandard discontinued the Russian Ladasten brand in 2018.
Who should avoid Bromantane?
Avoid Bromantane if you are pregnant or lactating, under 18, on an MAOI, or competing in any tested sport. WADA has Bromantane on the Prohibited List (S6.A Stimulants) since 1997, with the original Atlanta 1996 doping cases triggering inclusion (Burnat 1997, Docherty 2008). Caution with other dopaminergics including modafinil, methylphenidate, amphetamines, L-DOPA, and selegiline. Bipolar I and uncontrolled hypertension are also reasonable contraindications given the dopaminergic activity, even though the trial cohort excluded these populations.
How fast should I see effects from Bromantane?
Subjective stimulation typically begins 1.5 to 2 hours after an oral dose and lasts 8 to 12 hours, with the half-life around 11.2 hours and Tmax of 2.75 hours in women and 4 hours in men (Oliynyk and Oh 2012). The Russian Ladasten label cites a therapeutic effect within 1 to 3 days. Full asthenic relief in clinical trials manifested over 1 to 2 weeks (Voznesenskaia 2010). Therapeutic benefit persisted at least one month after discontinuation, which is consistent with a gene-induction mechanism that outlasts plasma drug exposure.
Bromantane vs Modafinil vs Selank: which fits which use case?
Bromantane fits asthenic recovery and stress resilience; Modafinil fits acute wakefulness with stronger Western RCT support; Selank fits anxiolysis with a peptide route. Bromantane has a slower 1-to-2-hour onset and a longer 1-to-2-week ramp to full effect, while Modafinil is on within an hour and Selank intranasal is even faster. Modafinil is FDA-approved with formal cognitive-battery RCTs, which is why it scores 5.8 / 10. Bromantane scores 6.3 / 10 with a stronger native asthenia signal but a thinner Western evidence base (Pharmstandard discontinued the only registered brand).
Where does the Bromantane score come from, and what would change it?
The 6.3 reflects an Evidence dimension of 2.0 / 5.0 after a 1.0-point downward integrity adjustment for industry funding combined with two industrial actors withdrawing from development. Pharmstandard discontinued Ladasten manufacturing in 2018 and the Russian registration lapsed, and Algernon Pharmaceuticals retired the NP-160 program after announcing positive but never-peer-reviewed 2019 NASH and CKD preclinical data. A Western Phase II RCT with a positive primary endpoint would reverse the integrity adjustment and lift the score by 1.0 to 1.5 points; an independent replication of the Voznesenskaia 2010 outcome would lift it by 0.5 to 1 point.
What could change Bromantane (Ladasten)'s score?
BioHarmony scores are living assessments. New research, regulatory changes, or personal context can shift the score up or down. These are the most likely scenarios that would change this intervention's rating.
The most plausible score-moving event is a Western Phase II RCT with a positive primary endpoint, which would reverse the 1.0-point integrity adjustment and lift Evidence from 2.0 to 3.0 or 3.5. That alone would lift the overall score by approximately 1.0 to 1.5 points. An independent replication of the Voznesenskaia 2010 outcome by a non-Pharmstandard, non-Zakusov-Institute group would lift Evidence by 0.5 to 1.0 points and push Efficacy higher. A documented long-term (greater than 6 months) safety signal would either rescue Safety to 2.0 (if reassuring) or sink it to 3.5 (if a tolerance or downregulation pattern emerged). The first three scenarios are plausible within 24 to 36 months; the rest require larger industrial commitment that does not appear imminent given Pharmstandard and Algernon both walking away.
| Scenario | Dimension shifts | New Score |
|---|---|---|
| Western Phase II RCT positive on cognition or asthenia primary endpoint | Evidence 2.0 → 3.5, Efficacy 3.5 → 4.0 | 7.2 / 10 💪 Strong recommend |
| Independent replication of Voznesenskaia 2010 outside Russia | Evidence 2.0 → 2.8, Efficacy 3.5 → 3.8 | 6.9 / 10 👍 Worth trying |
| Long-term (greater than 6 months) human safety study clean | Safety 2.5 → 2.0, Reversibility 1.5 → 1.0 | 7.2 / 10 💪 Strong recommend |
| New Western manufacturer with FDA breakthrough designation | Evidence 2.0 → 3.5, Cost 3.0 → 2.0 | 7.2 / 10 💪 Strong recommend |
| Tolerance pattern documented in 6-month human trial | Durability 3.5 → 2.0, Dependency 2.0 → 3.0 | 6.4 / 10 👍 Worth trying |
| Major late-stage AE signal or population-level hepatotoxicity | Safety 2.5 → 4.0, Reversibility 1.5 → 3.0 | 5.2 / 10 ⚖️ Neutral |
Key Evidence Sources
- Voznesenskaia TG, Fokina NM, Iakhno NN. Treatment of asthenic disorders in patients with psychoautonomic syndrome. Zh Nevrol Psikhiatr Im S S Korsakova. 2010.. Flagship Russian Phase III multicenter trial. n=728 outpatients, 50 to 100 mg/day for 28 days. CGI-S responder 76.0%, CGI-I responder 90.8%, AE 3%, discontinuation 0.8%.
- Neznamov GG et al. Ladasten in treatment of neurasthenia (placebo-controlled comparative study). Zh Nevrol Psikhiatr Im S S Korsakova. 2009.. Only published placebo-controlled Bromantane RCT. 28 days plus 1-week washout. No withdrawal syndrome.
- Mikhaylova M et al. Effects of ladasten on dopaminergic neurotransmission and hippocampal synaptic plasticity in rats. Neuropharmacology. 2007.. Most rigorous mechanistic paper. D1/D5-dependent hippocampal LTP transformation. Only Western-journal placement.
- Vakhitova YV et al. Cytosine demethylation in the TH gene promoter in hypothalamic cells under the action of ladasten. Genetika. 2006.. Epigenetic activation of TH transcription. Strongest mechanistic finding.
- Salimgareeva MK et al. Activation of gene expression for neurotrophins and MAP kinases. Bull Exp Biol Med. 2012.. Canonical BDNF and NGF mRNA paper. pERK1/2 up 70% at 0.5 h.
- Vakhitova YV et al. Ladasten induces expression of genes regulating dopamine biosynthesis. Eksp Klin Farmakol. 2004.. TH and DDC gene activation in striatum and hypothalamus.
- Neznamov GG et al. Characteristics of ladasten effect in neurasthenia patients with various EEG parameters. Eksp Klin Farmakol. 2008.. EEG-stratified responder analysis showing dual mechanism: psychostimulant or anxiolytic by baseline alpha.
- Oliynyk S, Oh S. The pharmacology of actoprotectors. Biomol Ther (Seoul). 2012.. Closest Western touchpoint. Korean narrative review (not systematic). Heat, hypoxia, CO, fatigue protection.
- Morozov IS et al. The mechanisms of the neurotropic action of bromantan. Eksp Klin Farmakol. 1999.. Landmark mechanism review.
- Tallerova AV et al. Effect of ladasten on cytokine markers in mice with depression-like syndrome. Bull Exp Biol Med. 2011.. Animal anti-depressant signal. More potent than imipramine on TNF-alpha and IL-6.
- Iezhitsa IN et al. 2-month bromantane course in rats. Eksp Klin Farmakol. 2000.. Closest animal analog to the missing >28-day human safety data. Recovery within 2 months; no tolerance.
- Morozov IS, Kleimenova NN. Bromantane increases physical work capacity in mice and rats. Eksp Klin Farmakol. 1998.. Effect 1.3 to 1.6 times phenamine; >24 h duration.
- Burnat P et al. Bromontan, a new doping agent. Lancet. 1997.. Western recognition came through Atlanta 1996 doping cases, not therapeutics.
- Docherty JR. Pharmacology of stimulants prohibited by WADA. Br J Pharmacol. 2008.. Bromantane Table 1: serotonergic and dopaminergic. Atlanta plus Sydney positives.
- Vanhee C et al. Multi-laboratory European/Australian surveillance of illicit nootropics. J Xenobiot. 2025.. Bromantane detected in 2 illicit samples; one at 33.2 mg per unit (underdose datapoint).
- Tanz LJ et al. US stimulant overdose deaths, January 2018 through June 2024. MMWR. 2025.. Bromantane footnote-only in stimulant definitions. No US overdose mortality signal.
- WADA 2025 Prohibited List.. Bromantane on S6.A Stimulants every annual list since 1997.
What does the evidence say about Bromantane (Ladasten)?
Evidence on this intervention is summarized across three complementary streams: contemporary clinical research, pre-RCT-era pharmacology and observational use, and the traditional medical systems that documented it first. Convergence across streams signals higher confidence; divergence is surfaced honestly.
Modern Clinical Research
Confidence: Limited
On the Outliyr Podcast, Awais Spall noted: “I personally really like bromentane it increases dopamine but without doing it in a destructive habit-forming way it inhibits the enzyme that breaks down dopamine.” (EP96).
Citations: Voznesenskaia 2010, Neznamov 2009, Mikhaylova 2007, Salimgareeva 2012, Vakhitova 2006, Oliynyk 2012
Pre-RCT-Era Pharmacology and Use
Confidence: Emerging
Citations: PMID 10222828, PMID 10998997, Morozov 1998
Traditional Medicine Systems
Holistic Evidence for Bromantane (Ladasten)
The modern lens and the historical operational lens point in the same direction: a clinically real but narrowly studied actoprotector with a coherent mechanism story and a thin RCT base. Convergence does not increase confidence here because both lenses trace back to the same Russian institutional consortium.
What to Track If You Try This
These are the data points that matter most while running a 30-day Experiment with this intervention.
How to read this section
- Pre
- Test or score before starting the protocol. Anchors a baseline.
- During
- Track while running the protocol so you can see if anything is changing.
- Post
- Re-test after a full cycle to confirm the change held.
- Up
- The marker should rise. For most positive outcomes, that is a good sign.
- Down
- The marker should fall. For most positive outcomes, that is a good sign.
- Stable
- The marker should hold steady. Big swings in either direction are a yellow flag.
- Watch
- Direction depends on dose, timing, and your baseline. Pay close attention to the trend.
- N/A
- No expected direction. The entry is there to anchor a baseline reading.
- Primary
- The Pulse dimension most likely to shift. Track this first.
- Secondary
- Also relevant, but a smaller or less consistent shift. Track if Primary is unclear.
Bloodwork to Order
Open These Markers In Your Dashboard
- ALT Baseline (pre-protocol) During | Expected Stable
- AST During | Expected Stable
- Cortisol AM Baseline (pre-protocol) During | Expected Watch
- Prolactin During | Expected Down
Pulse Dimensions to Watch
- Energy During | Expected Up | Primary
- Drive During | Expected Up | Primary
- Calm During | Expected Up | Secondary
- Sleep During | Expected Down | Secondary
Subjective Signals (Daily Voice Card)
- Focus Duration Scale 1-5 | During | Expected Up
- Stress Recovery After Hard Days Scale 1-5 | During | Expected Up
- Sleep Latency Scale 1-5 | During | Expected Watch
- Agitation Or Irritability Scale 1-5 | During | Expected Watch
Red Flags: Stop and Consult
- Persistent insomnia, agitation, or dysphoria at any dose
- Resting heart rate or blood pressure trending up over 4 weeks
- Any tested-sport competition (WADA prohibited list)
- Pregnancy, lactation, or active psychiatric instability
Other interventions for Cognition & Focus
See all ratings →📊 How BioHarmony scoring works
BioHarmony translates a weighted expected-value calculation into a reader-facing 0–10 score. Tier bands: Skip 0–2.9, Caution 3.0–4.4, Neutral 4.5–5.7, Worth Trying 5.8–6.9, Strong Recommend 7.0–8.7, Top-tier 8.8–10.0.
Harm-type downsides (safety risk, side effects, reversibility, dependency) carry a 1.4× precautionary multiplier. Harm weighs more than benefit. Opportunity-type downsides (financial cost, time/effort, opportunity cost) are subtracted at face value.
Use case subratings are independent assessments of how well the intervention addresses specific health goals. They are not components of the overall score. Each subrating reflects the scorer's judgment based on use-case-specific evidence, safety, and effect sizes.
Every dimension is evaluated on a 1–5 scale, and the baseline (1) is subtracted before weighting. A perfect intervention with zero downsides contributes zero penalty rather than a residual floor, so top-tier scores are actually reachable.
EV = Upside − Downside
EV = 2.540 − 0.892 = 1.648
Formula v2.0 maps EV = 0 to score 5.0. Above neutral, EV = +4.00 reaches 10.0; below neutral, EV = −5.36 reaches 0.0. Both sides use the full 5-point half-scale.
Score = 5 + (1.648 / 4.00) × 5 = 7.1 / 10