MA-5

Mitochonic acid 5 — 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid; a synthetic derivative of the plant hormone indole-3-acetic acid, from Takaaki Abe's group at Tohoku University. Binds mitofilin/Mic60. NOT an indole-3-propionic acid compound and not related to IPAM

MA-5 (Mitochonic acid 5 — 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid; a synthetic derivative of the plant hormone indole-3-acetic acid, from Takaaki Abe's group at Tohoku University. Binds mitofilin/Mic60. NOT an indole-3-propionic acid compound and not related to IPAM) is a longevity & bioregulators research compound. A mitochondria-homing small molecule that works on the shape of the inner membrane rather than on the respiratory chain. MA-5 binds mitofilin (Mic60) at the crista junction, the core component of the mitochondrial inner-membrane organizing system, and that binding facilitates oligomerization of ATP synthase and supercomplex formation — which raises local ATP production and lowers mitochondrial reactive oxygen species without changing the activity of complexes I through IV. That is the unusual claim: it is not an antioxidant, not an uncoupler and not a biogenesis agent, and it raises ATP even when oxidative phosphorylation or electron transport is pharmacologically inhibited. It was found by screening an in-house library of analogs of the plant hormone indole-3-acetic acid for ATP elevation in Hep3B cells, so its parent scaffold is an auxin rather than a human metabolite. Downstream effects reported in models are reduced mitochondrial fragmentation, restored crista shape, and suppression of GDF-15 release under oxidative stress.

How MA-5 works

A mitochondria-homing small molecule that works on the shape of the inner membrane rather than on the respiratory chain. MA-5 binds mitofilin (Mic60) at the crista junction, the core component of the mitochondrial inner-membrane organizing system, and that binding facilitates oligomerization of ATP synthase and supercomplex formation — which raises local ATP production and lowers mitochondrial reactive oxygen species without changing the activity of complexes I through IV. That is the unusual claim: it is not an antioxidant, not an uncoupler and not a biogenesis agent, and it raises ATP even when oxidative phosphorylation or electron transport is pharmacologically inhibited. It was found by screening an in-house library of analogs of the plant hormone indole-3-acetic acid for ATP elevation in Hep3B cells, so its parent scaffold is an auxin rather than a human metabolite. Downstream effects reported in models are reduced mitochondrial fragmentation, restored crista shape, and suppression of GDF-15 release under oxidative stress.

Proposed benefits

Researched for mitochondrial ATP production, crista structure and cell survival in mitochondrial disease models, and now in a clinical trial for hearing loss in mitochondrial disease.

Where to get MA-5

The evidence for MA-5

Graded by what exists behind each claim.

✅ Clinically validated

• A phase 1 is complete, and its results are in a registry rather than a journal. jRCT2031210495, investigator-initiated by Tohoku University with dosing at the Showa University Clinical Research Institute: 58 healthy Japanese men aged 20-44 against a planned 56, oral MA-5 taken fasted, single doses in Part A and 7 consecutive days in Part B, running 18 January 2022 to 25 July 2023. Posted results: adverse events in 12.1% (7 of 58), no side effects attributed to the drug, no serious adverse events, no discontinuations for adverse events, exposure rising with dose and unchanged by repeated dosing. No publication exists — PubTator3 returns no phase 1 paper for this compound as of 29 September 2026.
• A phase 2 is running now, and it is small and specific. jRCT2031250505, registered 3 December 2025: an exploratory, placebo-controlled, double-blind, investigator-initiated Phase 2 in 15 patients aged 16-65 with mitochondrial disease accompanied by hearing loss, at four Japanese hospitals (Juntendo, Tohoku University, Tokyo Medical Center, Jichi Medical University). Oral dosing for 12 weeks followed by a 12-week observation period. The endpoints are the useful part: auditory brainstem response, pure-tone audiometry from 125 to 8000 Hz, distortion-product otoacoustic emissions, hearing-related quality-of-life questionnaires, and blood GDF-15, FGF21, lactate and pyruvate, with pharmacokinetics at weeks 0 and 4 and secondary measures including MMSE, 6-minute walk distance, grip strength, eGFR and cardiac function.
• What this does NOT amount to. A completed phase 1 establishes that healthy young men tolerated it for a week. It says nothing about efficacy, and the phase 2 has not reported. Anyone describing MA-5 as clinically supported is describing a trial that is underway, not a result. The dose levels used in the phase 1 also could not be read consistently from the registry (see the dose note), so the studied range is recorded here as not reliably read rather than quoted.

📊 Correlative data

• The human-tissue evidence is a fibroblast series, and it is the best-replicated part of the file. Across 25 patient fibroblast lines carrying various genetic mutations, 24 of 25 (96%) responded to MA-5. That is human cells from real patients rather than an immortalized line, and the breadth of genotypes is the point — the effect did not require a particular mutation. It is still a dish: no person was dosed.
• The original patient series named the diseases specifically: fibroblasts from patients with Leigh syndrome, MELAS, Leber's hereditary optic neuropathy and Kearns-Sayre syndrome survived stress better with MA-5, and survival tracked the rise in cellular ATP.
• GDF-15 is the bridge between the cells and the clinic, and it is already being used that way. MA-5 abrogated the significant increase in GDF-15 seen under oxidative stress, and the authors proposed GDF-15 as a useful diagnostic biomarker for clinical trials. The phase 2 now running lists blood GDF-15 and FGF21 among its endpoints — so the biomarker proposed in 2017 is the one being measured in patients in 2026, which is how a mechanism claim is supposed to mature.

🧪 Theoretical / extrapolated

• The binding target is named, localized and unusual. MA-5 targets mitofilin (Mic60) at the crista junction of the inner membrane, and overexpressing mitofilin in Hep3B cells raised basal ATP with MA-5 amplifying the effect. Mitofilin is the core of the mitochondrial inner-membrane organizing system — a structural protein, not an enzyme — so the claim is that MA-5 changes the geometry of the membrane the ATP synthase sits in.
• The downstream claim is oligomerization, and it explains the strangest observation. MA-5 facilitates ATP synthase oligomerization and supercomplex formation with mitofilin/Mic60, reduces mitochondrial ROS, reduces mitochondrial fragmentation and restores crista shape — without affecting the activity of complexes I-IV, and while raising ATP even when oxidative phosphorylation or the electron transport chain is inhibited. That is why the authors insist it is not an antioxidant therapy: it is not scavenging anything, it is making the machine that makes ATP pack together more efficiently.
• The mammalian in vivo record covers four organs and two injury models. In mito-mice carrying a large mtDNA deletion, MA-5 improved reduced cardiac and renal mitochondrial respiration and appeared to prolong survival — with the authors stating plainly that survival statistics could not be conducted. In an ischemia-reperfusion model and a cisplatin nephropathy model, MA-5 improved renal function. In a later mito-mouse study it inhibited progression of low body weight and lactic acidosis and protected renal respiration even when mutant mtDNA exceeded 80%. In transient middle-cerebral-artery occlusion in mice it reduced neurological deficits and infarct volume and suppressed the Bax/Bcl-2 ratio.
• The hearing result is the one the clinic followed. In Cdk5rap1-knockout mice, which develop early hearing loss through defective 2-methylthiolation of mitochondrial tRNAs, MA-5 improved auditory brainstem response thresholds and distortion-product otoacoustic emissions, reduced spiral-ganglion and outer-hair-cell loss, prevented mitochondrial degeneration in spiral ligament fibrocytes, raised SIRT1, promoted YAP nuclear translocation and reduced lactate accumulation. The phase 2's primary endpoints are the same two hearing measures used in that mouse study.
• Invertebrate work adds breadth and one clean mechanistic control. In C. elegans, 10 microM MA-5 attenuated age-related decline in motor performance, loss of muscle mitochondria and degeneration of dopaminergic neurons associated with mitochondrial calcium overload. In a Duchenne model it alleviated movement decline, muscle tone, mitochondrial fragmentation and calcium accumulation; against rotenone it suppressed ROS, network fragmentation, nuclear destruction and ATP decline, and it protected dopaminergic CEP neurons. Most usefully, it reduced mitochondrial swelling caused by an immt-1 null mutation — immt-1 being the worm's mitofilin, which is the closest thing in this file to a genetic test of the proposed target.

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What MA-5 actually does

This molecule works on the shape of a membrane, not on the chemistry of a reaction, and that is what makes it worth a page. Suzuki 2015 names it in full: MA-5 is 4-(2,4-difluorophenyl)-2-(1H-indol-3-yl)-4-oxobutanoic acid. Count the atoms in that name and you get C₁₈H₁₃F₂NO₃, a molecular weight of 329.3 g/mol: an indole ring, a four-carbon acid chain, a ketone, and a difluorinated benzene ring. It was found by screening an in-house library of analogs of the plant hormone indole-3-acetic acid for ATP elevation in Hep3B human cells, so its scaffold is an auxin — a plant growth regulator — rather than anything a human body makes.

One structural detail nobody in this category prints: there is a stereocenter at C-2. The indol-3-yl group and the hydrogen sit on the same carbon, so MA-5 exists as two enantiomers. The completed phase 1 listed MA-5 enantiomers among its secondary endpoints, which means the investigators treated the two forms as pharmacologically distinct and measured them separately. A capsule sold as 3 mg of MA-5 may be racemic; nothing on any vendor page states which.

The target is a structural protein at a specific location. Suzuki 2016 reports that MA-5 targets the mitochondrial protein mitofilin at the crista junction of the inner membrane. Mitofilin (also Mic60) is the core component of the mitochondrial inner-membrane organizing system — the scaffold that holds the cristae folded and pinches their entrances. It is not an enzyme and it has no catalytic site, so this is a binding event that changes geometry.

What that geometry buys is packing, and the packing is the mechanism. Matsuhashi 2017 shows MA-5 facilitating ATP synthase oligomerization and supercomplex formation with mitofilin/Mic60, reducing mitochondrial fragmentation, and restoring crista shape and dynamics. ATP synthase works better when it is dimerized and rowed along a tightly curved crista ridge, because that curvature concentrates the proton gradient where the enzyme sits. Change the fold, change the local proton concentration, get more ATP out of the same respiratory chain.

The observation that rules out the obvious alternatives. Suzuki 2016 states that MA-5 facilitated ATP production and reduced mitochondrial ROS without affecting the activity of mitochondrial complexes I–IV, and Suzuki 2015 adds that it enhanced survival even when oxidative phosphorylation or the electron transport chain was inhibited. So it is not a complex-I agonist, not an uncoupler, not a biogenesis agent and — the authors are emphatic — not an antioxidant. The ROS reduction is a consequence of a better-organized membrane, not of scavenging. The nearest genetic confirmation is in a worm: Wu 2022 found MA-5 reduced mitochondrial swelling caused by an immt-1 null mutation, immt-1 being the C. elegans mitofilin.

One name collision worth closing. This is an indole-3-ACETIC acid derivative with a difluorophenyl ketone bolted on, and its claim is mitofilin binding. It is not indole-3-propionic acid, not indolepropionamide, and it shares nothing with those beyond the indole ring — whose only role here is as a mitochondria-homing scaffold.

Cell, rodent, human — and where it stops

This chain is longer than almost anything else in this catalog — human cells, four mammalian models, two invertebrate models, a completed phase 1 and a running phase 2 — and it has one structural weakness that runs the whole length of it.

Human cells, and this is the strongest link. Suzuki 2015 took fibroblasts from patients with Leigh syndrome, MELAS, Leber's hereditary optic neuropathy and Kearns-Sayre syndrome and showed improved survival under stress with MA-5, tracking a rise in cellular ATP. Matsuhashi 2017 then scaled it: 25 patient fibroblast lines carrying various mutations, of which 24 (96%) responded. Human tissue, real mutations, one lab.

Mouse, model one — the genetic disease model. Mito-mice carry an accumulating large mtDNA deletion that mimics human mitochondrial disease. Suzuki 2016 reported MA-5 improving reduced cardiac and renal mitochondrial respiration and “seemed to prolong survival, although statistical analysis of survival times could not be conducted” — the authors' own words, and exactly the sentence a vendor page would drop. Ogasawara 2026 returned to the same model and found MA-5 inhibited the progression of low body weight and lactic acidosis and protected renal respiration and function even when mutant mtDNA accumulated above 80%, while also resolving the cardiac respiration defect.

Mouse, models two and three — acquired injury. In ischemia-reperfusion and cisplatin nephropathy, MA-5 improved renal function Suzuki 2016. In transient middle-cerebral-artery occlusion, from a group independent of the originating lab, MA-5 reduced neurological deficits and infarct volume and suppressed the rise in the Bax/Bcl-2 ratio, with ATP-coupled respiration raised in SH-SY5Y cells after oxygen-glucose deprivation Sasaibe 2025.

Mouse, model four — the one the clinic followed. Cdk5rap1-knockout mice lose hearing early because a mitochondrial tRNA modification is defective. MA-5 improved ABR thresholds and distortion-product otoacoustic emissions, reduced spiral-ganglion and outer-hair-cell loss, prevented mitochondrial degeneration in spiral ligament fibrocytes, raised SIRT1, promoted YAP nuclear translocation and reduced lactate Kouga 2025. Those two hearing measures are now the primary endpoints of the human phase 2.

Invertebrates, which add breadth and the target control. 10 µM MA-5 attenuated age-related motor decline, muscle mitochondrial loss and dopaminergic degeneration tied to mitochondrial calcium overload in C. elegans Wu 2023; in Duchenne and rotenone-Parkinson's models it alleviated movement decline, fragmentation, ROS and ATP loss, and reduced swelling from an immt-1 null — the mitofilin gene Wu 2022.

Humans. The phase 1 (jRCT2031210495) dosed 58 healthy Japanese men aged 20–44, fasted, single doses and 7 consecutive days, from January 2022 to July 2023: adverse events in 12.1% (7/58), none attributed as side effects, no serious events, no discontinuations. The phase 2 (jRCT2031250505, registered 3 December 2025) is dosing 15 patients aged 16–65 with mitochondrial disease and hearing loss at four Japanese hospitals, oral, 12 weeks plus a 12-week observation period, against ABR, pure-tone audiometry, DPOAE, hearing questionnaires and blood GDF-15, FGF21, lactate and pyruvate.

Now the weakness that runs the whole length of the chain, and it is the reason this page exists. Every single efficacy result above was obtained in a system whose ATP production was already broken — by an mtDNA deletion, by a patient's inherited mutation, by rotenone, by cisplatin, by ischemia, by a tRNA-modification knockout. The mechanism is a repair of a deficit. Nobody has published an experiment asking what MA-5 does in a mitochondrially normal animal or person, and the trial population had to be genetically diagnosed to qualify. A healthy buyer is not the organism in any of these papers, and the prediction from the mechanism itself is that there is nothing for it to fix.

MA-5 pharmacokinetics — how much of it actually gets in

The pharmacokinetics were measured in humans and then not published, which is a different problem from not being characterized. The completed phase 1 (jRCT2031210495) had as a primary endpoint plasma and urinary MA-5 concentrations and pharmacokinetic parameters, plus MA-5 enantiomers and metabolites as secondary endpoints. Those numbers exist in a data set held by Tohoku University. A PubTator3 search on 29 September 2026 returns no phase 1 publication for this compound, so no C_max, no T_max, no half-life and no bioavailability figure can be quoted from the literature. Saying the kinetics are uncharacterized would be wrong; saying they are unpublished is the accurate sentence.

What the registry does state bounds the half-life. The posted results say exposure rose dose-dependently and that repeated dosing had no effect on it. No accumulation across 7 consecutive daily doses means the drug is substantially cleared inside each 24-hour interval — four to five half-lives inside a day puts it in the range of about 5 hours or less. That is arithmetic performed here from the registry's own statement, not a measured value, and it is the honest substitute for a number nobody has printed.

The chemistry predicts the rest, and it predicts one specific obstacle. MA-5 is a carboxylic acid with a pK_a in the low single figures, so at blood pH it circulates almost entirely as an anion. Anions are highly albumin-bound, distribute poorly into cells by passive diffusion, and are handled by the organic-anion transporters of the proximal tubule — which is both why the phase 1 measured urinary drug and why the kidney is where almost every efficacy result in this file sits Suzuki 2016 Ogasawara 2026. The awkward corollary is the central nervous system: a charged organic acid should enter the brain and the inner ear badly, and yet the hearing Kouga 2025 and stroke Sasaibe 2025 results say something reached those tissues in a rodent. Nobody has published a brain-to-plasma or cochlea-to-plasma ratio for MA-5 in any species, and that single measurement is the gap between those two papers and a mechanism.

Dosing conditions are not a footnote here. The phase 1 dosed fasted, in both the single-dose and the 7-day repeated-dose parts. For a weak acid, gastric pH governs the fraction absorbed in the un-ionized form, so food — and anything that raises gastric pH — is a plausible exposure variable that has never been tested. Fasted is the only condition with human data behind it.

The exposure numbers that do exist are concentrations in dishes, and they are not doses. Wu 2023 used 10 µM in the worm medium. The abstracts of the mammalian studies read here give no mg/kg and no route. So no allometric conversion is offered on this page: converting a bath concentration into a human milligram figure would be arithmetic with nothing underneath it. What can be said is the practical arithmetic: the vendor sells 3 MG capsules, 60 per bottle, 180 MG total, and one capsule sits below the lowest dose level that appeared in either read of the phase 1 registry record.

What would have to be true, and how you would know it was not

Four predictions. Three name markers the compound's own clinical trial is already measuring; the fourth is the one that cuts against buying it.

1. If MA-5 engages mitochondrial stress signaling in a person, GDF-15 falls — but only if it was high to begin with. Matsuhashi 2017 showed GDF-15 rising significantly under oxidative stress and MA-5 abrogating that rise, and proposed GDF-15 as a diagnostic biomarker for clinical trials. The running phase 2 measures blood GDF-15 and FGF21. Both are orderable. The prediction has a direction and a floor: elevated GDF-15 and FGF21 should fall over 4–12 weeks; normal values cannot fall, so a healthy person measuring them will see noise and call it a null result when it is actually a floor effect. Draw both at baseline or do not draw them at all.

2. Lactate is the cheap version of the same test. MA-5 inhibited the progression of lactic acidosis in mito-mice Ogasawara 2026 and reduced lactate accumulation in the cochlea of hearing-loss mice Kouga 2025, and the phase 2 measures blood lactate and pyruvate. In someone with a genuine oxidative-phosphorylation defect, resting lactate is the marker most likely to move and the window is weeks. In someone without one, resting lactate is normal and stays normal.

3. The hearing prediction, which is the most specific claim any mitochondrial compound in this catalog makes. The mouse result was better ABR thresholds and DPOAE with preserved outer hair cells Kouga 2025, and the human trial's primary endpoints are pure-tone audiometry from 125 to 8000 Hz, ABR and DPOAE over 12 weeks. An audiogram is a real instrument, widely available, repeatable and quantitative. If MA-5 does anything in a person that person can verify, this is it — and the honest caveat is that the trial enrolls patients whose hearing loss comes from a diagnosed mitochondrial disease, not from noise or age alone.

4. THE PREDICTION THAT CUTS AGAINST THE PRODUCT, and it comes from the mechanism rather than from skepticism. The proposed mechanism is the correction of a deficit: better crista geometry, better ATP synthase oligomerization, more ATP where ATP was short Suzuki 2016 Matsuhashi 2017. In a person whose mitochondria are intact, oxidative phosphorylation is not the rate-limiting step for anything they can feel, so the prediction is no measurable change in anything — not GDF-15, not lactate, not an audiogram, not grip strength or 6-minute walk distance, the two functional measures the phase 2 itself uses. Add the dose arithmetic and the prediction sharpens: one 3 mg capsule is below the lowest dose level appearing in the phase 1 registry record, so a null result at one capsule a day would not even be a test of the compound. The falsification is symmetric and worth stating: if a healthy person on 3–6 mg a day does see GDF-15 or lactate move, the interesting question becomes what else is in the capsule.

What nobody has tested yet

Five experiments nobody has published, and the first one is embarrassing for how easy it would be.

1. The phase 1 paper. A 58-subject first-in-human study with plasma and urinary drug levels, metabolite profiling and separated enantiomers finished on 25 July 2023, and as of 29 September 2026 its only public form is a registry record. Nobody outside the sponsor can read a C_max, a half-life, a bioavailability estimate or a metabolite identity for this compound. Every dosing statement anyone makes about MA-5, including the one on this page, is therefore built on a summary rather than on data.

2. Anything at all in a healthy organism. Fibroblasts from patients Suzuki 2015 Matsuhashi 2017, mito-mice Suzuki 2016 Ogasawara 2026, rotenone worms Wu 2022, cisplatin and ischemic kidneys, occluded arteries Sasaibe 2025, a tRNA-modification knockout Kouga 2025. No published study asks what MA-5 does to a normal mitochondrion in a normal animal. One cohort of wild-type mice on the compound for three months, with respirometry and a metabolic panel, would tell a healthy buyer more than the entire disease literature does.

3. Which enantiomer does the work. The C-2 stereocenter means there are two molecules in the bottle unless somebody resolved them. The phase 1 measured enantiomers separately, so the question was live enough to put in the protocol, but no published experiment compares the two for mitofilin binding, ATP elevation or exposure. If one enantiomer carries the activity, every dose in the literature is effectively half of what it says.

4. Whether it reaches the brain and the inner ear, and at what fraction. Two papers report central and cochlear effects in rodents Kouga 2025 Sasaibe 2025 while the molecule is an organic acid that should cross membranes poorly. No brain-to-plasma or cochlea-to-plasma ratio has been published in any species. Until it is, the hearing result and the stroke result are outcomes without an exposure.

5. Chronic architecture. Mitofilin/Mic60 is structural, present in every mitochondrion of every tissue, and the proposed mechanism is to change how tightly the cristae fold and how ATP synthase packs Matsuhashi 2017. No study has held a mammal on MA-5 for a year and then looked at crista morphology, mitochondrial DNA copy number or tumor incidence. The longest human exposure on record is seven days and the longest planned is twelve weeks. For a compound bought as a daily longevity capsule, that is the entire question and nobody has asked it.

MA-5 — its own safety story, not its class's

The safety read here is better than almost anything comparable in this catalog, and its boundaries are exactly as narrow as the trial that produced it. The phase 1 (jRCT2031210495) posted adverse events in 12.1% (7 of 58) with no side effects attributed to the drug, no serious adverse events and no discontinuations, concluding that the investigational drug was safe and well tolerated. That cohort was 58 healthy Japanese men aged 20–44, fasted, for up to 7 days. No women. Nobody over 44. Nobody with the disease. Nobody for longer than a week. Every one of those is a real limit on what the 12.1% figure covers.

The organ the investigators themselves watched was the kidney, and that is the most useful safety fact on this page. The phase 1's secondary endpoints were tubular injury markers — NAG, beta-2-microglobulin, L-FABP and NGAL. Nobody puts four tubular markers in a first-in-human protocol casually. The reason is mechanistic rather than ominous: MA-5 circulates as an anion, anions are concentrated by the organic-anion transporters of the proximal tubule, and the proximal tubule is the most mitochondria-dense segment of the nephron — which is also why it is where the compound's benefit shows up Suzuki 2016 Ogasawara 2026. The same transport that delivers the drug to its best tissue concentrates it in the cell type least able to tolerate a surprise. Mitigation: a CMP with eGFR at baseline and at 12 weeks, and a urine albumin-to-creatinine ratio if there is any existing kidney history.

The mechanism-specific risk is one nobody has measured, and it is about structure rather than toxicity. Mitofilin/Mic60 organizes the inner membrane of every mitochondrion in every tissue, and MA-5's proposed action is to change crista geometry so ATP synthase oligomerizes more readily Matsuhashi 2017. Increasing the efficiency of a structure is not obviously free: crista architecture also governs cytochrome c sequestration and therefore the threshold for apoptosis, which is precisely the axis the stroke paper measured as the Bax/Bcl-2 ratio Sasaibe 2025. In injury models shifting that threshold is protective. In a healthy tissue over years nobody knows, because the longest exposure anyone has run is 7 days in a person and a few months in a mouse.

What this compound is not, which is a safety point because the marketing invites the error. It is not an antioxidant, not a stimulant, not an uncoupler and not a mitochondrial biogenesis agent Suzuki 2016. It does not raise metabolic rate, does not act on beta-adrenergic signaling and has no published effect on heart rate or body temperature. There is nothing in its mechanism that predicts the acute felt effects people expect from an energy product, and a reader who takes more because they feel nothing is escalating a compound whose human dose-range record cannot even be read cleanly.

The substitution risk, which is the real one. The people in whom MA-5 has shown benefit had diagnosed mitochondrial disease — genotyped, with lactate, GDF-15 and FGF21 to match Matsuhashi 2017 Ogasawara 2026. Mitochondrial disease is diagnosed and managed by a specialist, the phase 2 is running in 15 patients at four university hospitals, and buying a 3 mg capsule is not a way into that pathway. Anyone whose reason for wanting this is fatigue should draw the boring markers first — a CMP, a CBC, ferritin, thyroid, A1c — because the compound's own trial design assumes a defect that most fatigue does not have.

And a supply-chain note that is unusually load-bearing. MA-5 has never been marketed anywhere, so there is no reference product, no label, no pharmacopeial monograph and no approved assay. It is a chiral molecule with no published enantiomeric specification, sold by a vendor who prints no CAS number, no formula and no purity figure on the product page. A certificate reporting 329 as a mass says nothing about which enantiomer, or in what ratio, you received.

Sources read for this page

• Suzuki T, Yamaguchi H, Kikusato M, Matsuhashi T, Matsuo A, Sato T, Oba Y, Watanabe S, Minaki D, Saigusa D, Shimbo H, Mori N, Mishima E, Shima H, Akiyama Y, Takeuchi Y, Yuri A, Kikuchi K, Toyohara T, Suzuki C, Kohzuki M, Anzai J, Mano N, Kure S, Yanagisawa T, Tomioka Y, Toyomizu M, Ito S, Osaka H, Hayashi K, Abe T. Mitochonic Acid 5 (MA-5), a Derivative of the Plant Hormone Indole-3-Acetic Acid, Improves Survival of Fibroblasts from Patients with Mitochondrial Diseases. Tohoku Journal of Experimental Medicine 2015;236(3):225-32 · PMID 26118651
• Suzuki T, Yamaguchi H, Kikusato M, Hashizume O, Nagatoishi S, Matsuo A, Sato T, Kudo T, Matsuhashi T, Murayama K, Ohba Y, Watanabe S, Kanno S, Minaki D, Saigusa D, Shinbo H, Mori N, Yuri A, Yokoro M, Mishima E, Shima H, Akiyama Y, Takeuchi Y, Kikuchi K, Toyohara T, Suzuki C, Ichimura T, Anzai J, Kohzuki M, Mano N, Kure S, Yanagisawa T, Tomioka Y, Toyomizu M, Tsumoto K, Nakada K, Bonventre JV, Ito S, Osaka H, Hayashi K, Abe T. Mitochonic Acid 5 Binds Mitochondria and Ameliorates Renal Tubular and Cardiac Myocyte Damage. Journal of the American Society of Nephrology 2016;27(7):1925-32 · PMID 26609120
• Matsuhashi T, Sato T, Kanno SI, Suzuki T, Matsuo A, Oba Y, Kikusato M, Ogasawara E, Kudo T, Suzuki K, Ohara O, Shimbo H, Nanto F, Yamaguchi H, Saigusa D, Mukaiyama Y, Watabe A, Kikuchi K, Shima H, Mishima E, Akiyama Y, Oikawa Y, Hsin-Jung HO, Akiyama Y, Suzuki C, Uematsu M, Ogata M, Kumagai N, Toyomizu M, Hozawa A, Mano N, Owada Y, Aiba S, Yanagisawa T, Tomioka Y, Kure S, Ito S, Nakada K, Hayashi KI, Osaka H, Abe T. Mitochonic Acid 5 (MA-5) Facilitates ATP Synthase Oligomerization and Cell Survival in Various Mitochondrial Diseases. EBioMedicine 2017;20:27-38 · PMID 28579242
• Wu X, Nagasawa S, Muto K, Ueda M, Suzuki C, Abe T, Higashitani A. Mitochonic Acid 5 Improves Duchenne Muscular Dystrophy and Parkinson's Disease Model of Caenorhabditis elegans. International Journal of Molecular Sciences 2022;23(17):9572 · PMID 36076995
• Wu X, Seida M, Abe T, Higashitani A. Mitochonic acid 5 attenuates age-related neuromuscular dysfunction associated with mitochondrial Ca2+ overload in Caenorhabditis elegans. npj Aging 2023;9(1):20 · PMID 37528117
• Kouga T, Miwa T, Wei FY, Sunami K, Tomizawa K. Mitochonic acid 5 mitigates age-related hearing loss progression by targeting defective 2-methylthiolation in mitochondrial transfer RNAs. Frontiers in Cellular Neuroscience 2025;19:1541347 · PMID 40260078
• Sasaibe S, Yoshioka Y, Kuse Y, Nakamura S, Shimazawa M. Mitochonic acid 5, an ATP production accelerator, protects against neurological damage in ischemic stroke. Brain Research 2025;1860:149664 · PMID 40339682
• Ogasawara E, Tani H, Suzuki C, Owada Y, Ogata M, Ishihara N, Abe T, Nakada K. Effects of an indole chemical, mitochonic acid 5, in a mouse model of mitochondrial disease onset. Scientific Reports 2026; volume and pages not present in the PubTator3 record · PMID 42270754

MA-5 — interference & stacking

Bloodwork to run alongside MA-5

Baseline first, then again at 8–12 weeks.

The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.

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MA-5 — frequently asked questions

What MA-5 is used for

MA-5 appears under 3 goals in the goal router.

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