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    J147 molecular structure

    J147

    NootropicsPhase 2

    Also known as: J-147, J 147, Curcumin-derived phenyl hydrazide, N-(2,4-dimethylphenyl)-2,2,2-trifluoro-N-((3-methoxyphenyl)methylideneamino)acetamide

    J147 is a synthetic phenyl hydrazide derived from curcumin, made at the Salk Institute for Biological Studies. It came out of a screening strategy that deliberately avoided the amyloid hypothesis: instead of selecting for affinity to one disease-specific target, the group screened compounds against several cell culture models of age-associated pathology.

    Half-Life: Not established in humans; the phase 1 study measured terminal half-life but has not reported results (NCT03838185). After oral dosing in mice, half-life was about 1.5 hours in plasma and 2.5 hours in brain, with oral bioavailability calculated at 28 percent and a brain to blood ratio of about 0.5 (PMID: 23673233).Route: Oral, Intravenous infusionMW: 350.34 g/molCAS: 1146963-51-0
    Last reviewed:
    Nootropics
    Category
    Phase 2
    Research Stage

    Overview

    Best Price Available

    Disguised Alpha logo

    Disguised Alpha

    $99.99

    60 capsules · capsule

    At A Glance

    Mechanism

    The molecular target of J147 is the mitochondrial alpha-F1-ATP synthase subunit ATP5A. Modest inhibition of ATP synthase increases intracellular calcium, which produces sustained calcium/calmodulin-dependent protein kinase kinase beta (CAMKK2) dependent activation of the AMPK and

    Half-Life
    Not established in humans; the phase 1 study measured terminal half-life but has not reported results (NCT03838185). After oral dosing in mice, half-life was about 1.5 hours in plasma and 2.5 hours in brain, with oral bioavailability calculated at 28 percent and a brain to blood ratio of about 0.5 (PMID: 23673233).
    Routes
    OralIntravenous infusion
    Potential Benefits
    Facilitated memory in normal rodents and prevented loss of synaptic proteins and cognitive decline in transgenic Alzheimer disease mice (PMID: 22194796)Rescued spatial navigational memory and contextual fear conditioning in 20-month-old APP/PS1 mice treated after pathology was already advanced, with induction of nerve growth factor and brain-derived neurotrophic factor (PMID: 23673233)Prevented age-associated drift in the hippocampal transcriptome and plasma metabolome in mice and extended lifespan in Drosophila through ATP synthase and the AMPK pathway (PMID: 29316249)Reduced cognitive decline and metabolic and transcriptional markers of aging in rapidly aging SAMP8 mice (PMID: 31742554)Reduced infarct volume and reduced tissue plasminogen activator associated brain hemorrhage in rat models of ischemic stroke (PMID: 35309561)Improved neurofunctional recovery and reduced acute neurodegeneration after controlled cortical impact injury in mice (PMID: 39245209)

    Overview

    J147 is a synthetic phenyl hydrazide derived from curcumin, made at the Salk Institute for Biological Studies. It came out of a screening strategy that deliberately avoided the amyloid hypothesis: instead of selecting for affinity to one disease-specific target, the group screened compounds against several cell culture models of age-associated pathology. The molecule that emerged was orally active, facilitated memory in normal rodents and prevented the loss of synaptic proteins and cognitive decline in a transgenic Alzheimer disease mouse model (PMID: 22194796). Unlike the racetams on this site, J147 was never a marketed drug anywhere and has always been an investigational compound; consumer-facing material is sold as a research chemical. The molecular target was identified in 2018 as the mitochondrial alpha-F1-ATP synthase subunit ATP5A. Modest inhibition of ATP synthase raises intracellular calcium, which produces sustained CAMKK2-dependent activation of the AMPK and mTOR pathway, a longevity mechanism conserved across species. In mice, J147 prevented age-associated drift in the hippocampal transcriptome and plasma metabolome, and it extended lifespan in Drosophila (PMID: 29316249). Related work found that J147 and a second Salk compound increased acetyl-CoA levels by inhibiting acetyl-CoA carboxylase 1 and reduced cognitive decline and markers of aging in rapidly aging SAMP8 mice (PMID: 31742554). The strongest preclinical result is the treatment design rather than the prevention design. Twenty-month-old APP/PS1 transgenic mice, at a stage where pathology was already advanced, were fed J147 for three months and showed improved spatial navigational memory in the water maze and rescued contextual fear conditioning, alongside induction of nerve growth factor and brain-derived neurotrophic factor (PMID: 23673233). Efficacy has also been reported in rat models of ischemic stroke, where J147 reduced infarct volume and reduced tissue plasminogen activator associated brain hemorrhage (PMID: 35309561), in mouse traumatic brain injury (PMID: 39245209) and in mouse diabetic neuropathy (PMID: 29122628). The animal safety package is unusually detailed for a compound at this stage. Single doses of 2 g/kg in rats and mice produced no acute toxicity, and the Ames test, the hERG assay and CYP3A4 assays were all negative (PMID: 23673233). Because phenyl hydrazides can in principle be metabolized to carcinogenic aromatic amines or hydrazines, the group specifically tested this and found that J147 is not metabolized to those products in human or mouse microsomes or in mouse plasma (PMID: 23582448). A separate panel in a rat hepatoma line put the sustained concentration expected to produce toxicity at about 90 micromolar (PMID: 25364619). Human data are the gap. A phase 1 randomized, double-blind, placebo-controlled single ascending dose study in 64 healthy young and elderly volunteers, sponsored by Abrexa Pharmaceuticals, completed in February 2020 with safety and pharmacokinetics as endpoints, and no results have been posted or published (NCT03838185). A phase 2 study of intravenous J147 combined with endovascular therapy in acute ischemic stroke began recruiting in July 2026 (NCT07430917). J147 is not approved anywhere and remains a research-use-only compound in the United States market.

    Potential Research Fields

    Alzheimer diseaseMitochondrial ATP synthaseBrain agingNeuroprotection

    Chemical Information

    IUPAC Name

    Not yet available

    CAS Number

    1146963-51-0

    Molecular Formula

    C18H17F3N2O2

    Molecular Mass

    350.34 g/mol

    Dosing & Protocols

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    Interactions

    Contraindications

    None established in humans. The published phase 1 protocol excluded volunteers with clinically significant cardiovascular, neurological, psychiatric, hepatic or renal disease, required them to avoid grapefruit and Seville oranges, and excluded anyone who had taken known hepatic or renal clearance altering agents in the preceding 30 days, which indicates sponsor concern about metabolic interactions (NCT03838185). Mechanism-based caution: the target is the mitochondrial alpha-F1-ATP synthase and the compound works by modest inhibition of that enzyme (PMID: 29316249), so it is a metabolic intervention rather than a neutral supplement, and cell work shows mitochondrial effects at high concentrations (PMID: 25364619). No pregnancy, lactation or drug interaction data exist in humans.

    Research Disclaimer

    This interaction data is compiled from published research and community reports. It may not be exhaustive. Always consult a healthcare professional before combining compounds.

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    t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists.
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    Aniracetam

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    Aniracetam is a pyrrolidinone in the racetam family, developed by Hoffmann-La Roche under the code Ro 13-5057.

    t½ About half an hour for the parent drug in humans. Plasma elimination half-life was 0.47 to 0.49 hours after a single 400 mg oral dose in 20 healthy male volunteers (PMID: 19025058). Aniracetam is extensively metabolized to N-anisoyl-GABA and anisic acid; in six elderly hospitalized patients with cerebrovascular disease and reduced creatinine clearance, metabolite half-life was 4 to 7 times longer than in young volunteers (PMID: 9062694).
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    Bemethyl (bemitil)

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    t½ Not established in humans; in healthy volunteers given a single 250 mg oral dose of the Metaprot capsule form, peak serum ethylthiobenzimidazole averaged 0.91 microg/mL at about 1.06 h, and no terminal half-life was reported (PMID: 21870773)
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    t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose)
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    View Full Dosage Guide →

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    Disguised Alpha logo

    Disguised Alpha

    $99.99

    1 vendors · 1 listings

    Research Score

    30

    0 PubMed studies

    Quality Indicators

    Data Completeness

    63%
    Description
    Mechanism of Action
    Chemical Data
    Dosing Protocols
    Safety Profile
    PubMed Studies
    Interactions
    Vendor Listings

    Quick Facts

    Half-Life

    Not established in humans; the phase 1 study measured terminal half-life but has not reported results (NCT03838185). After oral dosing in mice, half-life was about 1.5 hours in plasma and 2.5 hours in brain, with oral bioavailability calculated at 28 percent and a brain to blood ratio of about 0.5 (PMID: 23673233).

    Molecular Weight

    350.34 g/mol

    Administration

    Oral, Intravenous infusion

    CAS Number

    1146963-51-0

    Trial Phase

    Phase 2

    0

    Research Disclaimer

    This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.

    Frequently Asked Questions

    What is J147 used for in research?

    J147 is a synthetic phenyl hydrazide derived from curcumin, made at the Salk Institute for Biological Studies. It came out of a screening strategy that deliberately avoided the amyloid hypothesis: instead of selecting for affinity to one disease-specific target, the group screened compounds against several cell culture models of age-associated pathology. The molecule that emerged was orally active, facilitated memory in normal rodents and prevented the loss of synaptic proteins and cognitive decline in a transgenic Alzheimer disease mouse model (PMID: 22194796). Unlike the racetams on this site, J147 was never a marketed drug anywhere and has always been an investigational compound; consumer-facing material is sold as a research chemical.

    The molecular target was identified in 2018 as the mitochondrial alpha-F1-ATP synthase subunit ATP5A. Modest inhibition of ATP synthase raises intracellular calcium, which produces sustained CAMKK2-dependent activation of the AMPK and mTOR pathway, a longevity mechanism conserved across species. In mice, J147 prevented age-associated drift in the hippocampal transcriptome and plasma metabolome, and it extended lifespan in Drosophila (PMID: 29316249). Related work found that J147 and a second Salk compound increased acetyl-CoA levels by inhibiting acetyl-CoA carboxylase 1 and reduced cognitive decline and markers of aging in rapidly aging SAMP8 mice (PMID: 31742554).

    The strongest preclinical result is the treatment design rather than the prevention design. Twenty-month-old APP/PS1 transgenic mice, at a stage where pathology was already advanced, were fed J147 for three months and showed improved spatial navigational memory in the water maze and rescued contextual fear conditioning, alongside induction of nerve growth factor and brain-derived neurotrophic factor (PMID: 23673233). Efficacy has also been reported in rat models of ischemic stroke, where J147 reduced infarct volume and reduced tissue plasminogen activator associated brain hemorrhage (PMID: 35309561), in mouse traumatic brain injury (PMID: 39245209) and in mouse diabetic neuropathy (PMID: 29122628).

    The animal safety package is unusually detailed for a compound at this stage. Single doses of 2 g/kg in rats and mice produced no acute toxicity, and the Ames test, the hERG assay and CYP3A4 assays were all negative (PMID: 23673233). Because phenyl hydrazides can in principle be metabolized to carcinogenic aromatic amines or hydrazines, the group specifically tested this and found that J147 is not metabolized to those products in human or mouse microsomes or in mouse plasma (PMID: 23582448). A separate panel in a rat hepatoma line put the sustained concentration expected to produce toxicity at about 90 micromolar (PMID: 25364619).

    Human data are the gap. A phase 1 randomized, double-blind, placebo-controlled single ascending dose study in 64 healthy young and elderly volunteers, sponsored by Abrexa Pharmaceuticals, completed in February 2020 with safety and pharmacokinetics as endpoints, and no results have been posted or published (NCT03838185). A phase 2 study of intravenous J147 combined with endovascular therapy in acute ischemic stroke began recruiting in July 2026 (NCT07430917). J147 is not approved anywhere and remains a research-use-only compound in the United States market.

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    Research Tools

    Related Compounds

    View All

    9-Me-BC (9-Methyl-β-carboline)

    NootropicsPreclinical

    9-Methyl--carboline (9-Me-BC) is a synthetic -carboline alkaloid that has drawn nootropic-community interest for a preclinical property that is genuinely unusual among -carbolines: in rodent and cell-culture studies it appears to stimulate the dopaminergic phenotype - raising tyrosine hydroxylase, the number of differentiated dopamine neurons and dopamine content - while also showing neuroprotective, neurorestorative and anti-inflammatory effects, plus in-vitro MAO-A/MAO-B inhibition [PMID:17913302, PMID:20374418, PMID:32285253].

    t½ Not characterized in humans (no pharmacokinetic data). Community/anecdotal only: ~5-25 mg per day, oral. No validated or approved human dose exists.
    6 studiesView Profile

    Aniracetam

    NootropicsApproved (Italy)

    Aniracetam is a pyrrolidinone in the racetam family, developed by Hoffmann-La Roche under the code Ro 13-5057.

    t½ About half an hour for the parent drug in humans. Plasma elimination half-life was 0.47 to 0.49 hours after a single 400 mg oral dose in 20 healthy male volunteers (PMID: 19025058). Aniracetam is extensively metabolized to N-anisoyl-GABA and anisic acid; in six elderly hospitalized patients with cerebrovascular disease and reduced creatinine clearance, metabolite half-life was 4 to 7 times longer than in young volunteers (PMID: 9062694).
    PreclinicalView Profile

    Bemethyl (bemitil)

    NootropicsApproved (Russia)

    Bemethyl, known in the Russian literature as bemitil and sold in the region under names including Metaprot, Bemactor and Antihot, is 2-ethylthiobenzimidazole, normally handled as the hydrobromide salt.

    t½ Not established in humans; in healthy volunteers given a single 250 mg oral dose of the Metaprot capsule form, peak serum ethylthiobenzimidazole averaged 0.91 microg/mL at about 1.06 h, and no terminal half-life was reported (PMID: 21870773)
    PreclinicalView Profile

    Bromantane

    NootropicsRussia Approved

    Bromantane is an atypical psychostimulant and anxiolytic developed in the 1980s at the Zakusov Institute of Pharmacology of the Russian Academy of Medical Sciences, originally created as an adaptogen for Soviet military and elite athletic use and later approved in Russia for the treatment of neurasthenic and asthenic disorders under the trade name Ladasten.

    34 studiesView Profile

    Cyclazodone

    NootropicsPreclinical

    Cyclazodone is the N-cyclopropyl derivative of pemoline, a 4-oxazolidinone stimulant.

    PreclinicalView Profile

    Dihexa

    NootropicsPreclinical

    Dihexa is a synthetic peptide analogue of the angiotensin IV metabolite LVV-hemorphin-7, developed at Washington State University.

    t½ Not characterized in humans. Dihexa was engineered for metabolic stability (resistant to plasma and enzymatic degradation) and blood-brain-barrier penetration; in preclinical work its central procognitive effects appear to outlast its plasma presence. 5 to 40 mg oral per day (anecdotal range; no established human dose)
    1 studiesView Profile

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