Visomitin
SkQ1, Skulachev ions, plastoquinonyl decyltriphenylphosphonium, MitoVitan, MitoVitan Active, Exomitin, the same active in an eye drop and in three topicals
Visomitin (SkQ1, Skulachev ions, plastoquinonyl decyltriphenylphosphonium, MitoVitan, MitoVitan Active, Exomitin, the same active in an eye drop and in three topicals) is a longevity & bioregulators research compound. A plastoquinone head group tethered by a ten-carbon chain to a triphenylphosphonium cation. The cation is the delivery mechanism and it is the whole idea: a lipophilic positive charge is driven across membranes by the electrical potential they carry, and the mitochondrial inner membrane carries the largest potential in the cell, so the molecule accumulates there by electrophoresis rather than by any receptor. The plastoquinone then does what it does in a chloroplast — intercepts the lipid peroxidation chain in the membrane it is sitting in. Concentration is the whole safety argument, because the same charge that concentrates it will uncouple respiration if there is too much of it.
Visomitin quick facts
| Route | Topical |
| Frequency | Dosed as drops in the trials · Daily in the trials |
| Half-life | Not characterized in humans for the ophthalmic product |
| Forms | Topical |
| Evidence level | Registered in Russia as an eye drop — the only registered SkQ1 medicine anywhere. One published phase 2 trial in dry eye. Not FDA-approved. |
The eye drop is the only registered SkQ1 medicine in the world and the only presentation with a published controlled trial in people, and the trial that exists is a phase 2 in dry eye run to a Western standard with a controlled adverse environment chamber. The serum and the hydrogel sold beside it at the same price have nothing of the kind. The honest summary of the wider record is mixed rather than glowing: the same molecule failed to help in a mouse sepsis model, which is the sort of result a program with a real research culture publishes and a marketing operation does not.
How Visomitin works
A plastoquinone head group tethered by a ten-carbon chain to a triphenylphosphonium cation. The cation is the delivery mechanism and it is the whole idea: a lipophilic positive charge is driven across membranes by the electrical potential they carry, and the mitochondrial inner membrane carries the largest potential in the cell, so the molecule accumulates there by electrophoresis rather than by any receptor. The plastoquinone then does what it does in a chloroplast — intercepts the lipid peroxidation chain in the membrane it is sitting in. Concentration is the whole safety argument, because the same charge that concentrates it will uncouple respiration if there is too much of it.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Visomitin
Buy Visomitin at RUPharma →The evidence for Visomitin
Graded by what exists behind each claim.
✅ Clinically validated
- A published phase 2 safety and efficacy trial of SkQ1 ophthalmic solution in dry eye, run both in the ordinary environment and under a Controlled Adverse Environment challenge (Petrov 2016) — the methodology the US regulatory pathway for dry eye actually uses.
- No SkQ1 product holds a United States approval (Valdes-Arias 2024). The Russian registration is real and it is a different standard.
📊 Correlative data
- SkQ1 protected cornea against oxidative damage from ultraviolet irradiation and mechanical injury in animals (Zernii 2018) — local delivery to the surface it was applied to.
- A clean negative, published with Skulachev on the author list: SkQ1 and MitoTEMPO failed to exert a long-term beneficial effect in murine polymicrobial sepsis (Rademann 2017).
- The most recent extension away from the eye is osteoclast metabolism and bone loss through a STAT3/LDHB axis (Yuan 2025) — mechanistic animal and cell work, not a human result.
🧪 Theoretical / extrapolated
- The delivery mechanism is physics rather than biology: a lipophilic cation is driven into mitochondria by the membrane potential, roughly 150-180 mV negative inside, which predicts several hundred-fold accumulation with no receptor involved.
- The same charge is the toxicity. Above its useful range the molecule uncouples the mitochondria it concentrates into, which is why the registered ophthalmic strength is 0.000155%.
- The serum and hydrogel sold at the same price have no controlled human trial of any kind. What the phase 2 established, it established for an eye drop in an eye.
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 Visomitin actually does
The delivery system is the invention, and it runs on physics rather than on biology. SkQ1 is a plastoquinone head group joined by a ten-carbon linker to a triphenylphosphonium cation. A lipophilic cation crosses membranes and then accumulates wherever the electrical potential is most negative on the inside. The mitochondrial inner membrane holds a potential of roughly 150 to 180 mV, negative inside, and the Nernst relationship says a tenfold concentration gradient per 61 mV. That predicts accumulation of several hundred-fold inside mitochondria relative to cytosol, driven by charge alone with no receptor and no transporter involved.
What the head group does once it is there. Plastoquinone is the electron carrier plants use in photosynthesis, and in this context it acts as a chain-breaking antioxidant inside the lipid phase of the membrane it has concentrated into. Lipid peroxidation propagates through membranes as a radical chain; an antioxidant dissolved in water cannot reach it, which is the design problem the cation solves.
The same charge is the toxicity, and the concentration window is the whole safety story. A lipophilic cation moving down an electrical gradient carries charge across the membrane, and charge movement without a proton gradient is uncoupling. Above its useful range this molecule stops being an antioxidant and starts dissipating the membrane potential that concentrated it. The registered ophthalmic strength is 0.000155%, which is about 1.55 micrograms per milliliter — a formulation deliberately at the bottom of that window.
How it sits beside the other quinones on this shelf. Suarez-Rivero 2021 reviews the coenzyme Q10 analogs as a therapeutic family and is the right frame for reading this one: idebenone shortens the tail to gain absorption, and SkQ1 replaces the tail with a charge to gain targeting. Two different answers to the same problem, which is that swallowed coenzyme Q10 largely does not reach mitochondria. Ji 2021 sets out why the eye became the test bed for both.
Cell, rodent, human — and where it stops
The human rung exists, and this is the only presentation that has one. Petrov 2016 is a phase 2 safety and efficacy study of SkQ1 ophthalmic solution in dry eye, run both in the ordinary environment and under a Controlled Adverse Environment challenge — a chamber that standardizes humidity, airflow and visual tasking so that a dry eye signal can be provoked reproducibly. That is the methodology the United States regulatory pathway for dry eye actually uses, and running it is what separates this product from everything else on the Skulachev shelf.
What phase 2 is, and what it is not. A positive phase 2 establishes that a signal exists at a chosen dose in a selected population. It is not registration, and it is not a claim of effectiveness in practice. Valdes-Arias 2024 reviews what has actually been approved in the United States for dry eye and describes a field whose approvals rest on inflammation and neuronal pathways. No SkQ1 product holds a United States approval. The Russian registration is real and it is a different regulatory standard.
The animal rung includes a clean negative, and it is published by the people who would rather it were not. Rademann 2017 tested SkQ1 and MitoTEMPO in murine polymicrobial sepsis and found no long-term beneficial effect. Skulachev is on the author list. A research program that publishes its own null result is behaving like a research program, and that is worth saying on a page about a product sold as a longevity molecule.
The positive animal work is corneal and it is local. Zernii 2018 reports protection of cornea against oxidative damage from ultraviolet irradiation and mechanical injury. Local delivery to the surface it is applied to. Yuan 2025 is the most recent extension away from the eye — osteoclast metabolism and bone loss through a STAT3 and LDHB axis — and it is a mechanistic animal and cell study, not a human result.
Visomitin pharmacokinetics — how much of it actually gets in
What degrades it, and where. This is a small lipophilic cation rather than a peptide, so proteases are irrelevant; the routes that matter are cytochrome-mediated oxidation and conjugation in the liver, and the quinone head group cycling between its oxidized and reduced forms in whatever membrane it is sitting in. On the eye, the clearance that dominates is not metabolic at all: tear turnover removes roughly 16% of the tear volume per minute, so a drop's residence time on the ocular surface is measured in minutes.
The oral barrier, and why this product is a drop. Triphenylphosphonium compounds have been given orally in animal work, and the general problem with the class is that oral bioavailability and first-pass metabolism determine how much charged material reaches the systemic circulation, after which it distributes into whichever tissues have the highest mitochondrial density and the largest membrane potential — heart and skeletal muscle, not the eye. Putting it on the eye as a drop is a way of reaching the target tissue at a controlled concentration without asking the gut wall or the liver any questions at all.
The number that bounds the exposure. The registered strength is 0.000155%, which is 1.55 µg/ml. A typical eye drop is about 30 µl, so one drop delivers roughly 0.05 micrograms of active to the ocular surface, of which the fraction crossing the cornea is small. Compare that with the milligram-scale systemic doses used in the rodent studies Rademann 2017 and the difference is four to five orders of magnitude. Nothing about the eye drop can be reasoned from the systemic animal literature, in either direction.
No human half-life is published for the ophthalmic product, and there is no injection to anchor it. No pharmacokinetic study of SkQ1 in people has been published for any route, so there is no plasma curve, no ocular tissue concentration and no comparator given by injection. What can be said is the shape imposed by the eye: minutes of surface residence, a small transcorneal fraction, and a dosing interval set by that rather than by any measured elimination.
What would have to be true, and how you would know it was not
This product has no blood read-out, and inventing one would be worse than saying so. Dry eye is measured on the eye, so the falsification here is observational and it is specific.
what to watch. Two things, and they disagree with each other more often than people expect. The sign is corneal and conjunctival staining, tear break-up time, and Schirmer wetting, all of which an optometrist measures in ten minutes. The symptom is a validated questionnaire score — the Ocular Surface Disease Index takes four minutes and is free. Petrov 2016 is built on exactly this sign-and-symptom pairing, and the reason the Controlled Adverse Environment chamber exists is that neither is stable enough on its own.
how long before it means anything. Ocular surface trials run on scales of weeks to months because the epithelium turns over in roughly a week and inflammation resolves more slowly than that. A change in the first few days is the vehicle, the preservative or the act of instilling fluid onto a dry surface. Four weeks is the shortest interval at which a before-and-after comparison is worth making, and twelve is better.
what will fool you. Three things, in order of how often they do it. Dry eye fluctuates enormously with season, humidity, screen time and sleep, so an uncontrolled before-and-after captures the weather as readily as the drug. Any drop relieves symptoms briefly because it is a drop. And the sign-symptom correlation in dry eye is famously poor, so feeling better while staining worsens is a real and common pattern rather than a paradox.
Against the product, and it applies to two of the three SKUs. The serum and the hydrogel sold at the same price as the eye drop have no controlled human trial of any kind. Whatever Petrov 2016 establishes, it establishes for a 0.000155% ophthalmic solution instilled into an eye, and it transfers to a cosmetic serum on facial skin exactly as far as any other trial transfers to a different product at a different concentration on a different tissue, which is not at all.
What nobody has tested yet
No human pharmacokinetics exist for any SkQ1 product. Not for the drop, not for the serum, not for any oral form. That means no measured ocular tissue concentration, no plasma level after instillation, and no basis for saying whether ophthalmic use is purely local. A single study measuring aqueous humor and plasma after dosing would answer all three.
The phase 3 result is not in the literature this page can read. A phase 2 has been published Petrov 2016; no phase 3 report resolves in the same search, and no United States approval exists Valdes-Arias 2024. The honest reading of a drug that reached phase 2 in 2016 and holds no Western approval a decade later is that something did not go the way the sponsor hoped, and the specific reason has not been published where a reader can check it.
Nobody has tested the topical SKUs on skin. The serum, the concentrate and the hydrogel share an active with the drop and share nothing else — not the concentration, not the vehicle, not the tissue. There is no controlled trial of any of them, and the cosmetic endpoints that would settle it are the same ones every serum on this site is measured by.
Extrapolation, labeled as such. If the mechanism is potential-driven accumulation, then the tissues with the highest mitochondrial density should show the largest effect and the largest risk. Yuan 2025 finding an osteoclast effect is consistent with that and is also a warning shape: a molecule that concentrates by charge does not stop at the tissue you aimed it at.
Visomitin — its own safety story, not its class's
Three things specific to a mitochondria-targeted cation.
The dose window is the mechanism, not a formality. The same electrochemical gradient that concentrates this molecule inside mitochondria means that above its useful range it uncouples them. That is not an idiosyncratic toxicity, it is the pharmacology run past its optimum, and it is the reason the registered ophthalmic product sits at 0.000155%. Concentrating a topical product, layering several of them, or reasoning from an animal study's milligram doses are all ways of leaving that window.
The published negative is part of the safety picture. Rademann 2017 found no long-term benefit in murine sepsis with Skulachev as an author. A reader deciding what to believe about this molecule should weigh that the program publishes its own failures — which raises confidence in the positive results and lowers the prior that a broad antioxidant is quietly fixing everything.
Eye drops carry an ordinary hazard the mechanism has nothing to do with. Any topical ophthalmic product can cause stinging, blurring and hypersensitivity, and contamination of the bottle tip is a real route to keratitis. Sudden eye pain, light sensitivity, discharge or a change in vision are reasons to stop and be examined rather than to persist with a course. Nothing on this page is a diagnosis or a substitute for an eye examination.
Sources read for this page
- Petrov A, Perekhvatova N, Skulachev M, Stein L, Ousler G. SkQ1 Ophthalmic Solution for Dry Eye Treatment: Results of a Phase 2 Safety and Efficacy Clinical Study in the Environment and During Challenge in the Controlled Adverse Environment Model. Advances in Therapy 2016 · PMID 26733410
- Rademann P, Weidinger A, Drechsler S, Meszaros A, Zipperle J, Jafarmadar M, Dumitrescu S, Hacobian A, Ungelenk L, Rostel F, Kaszaki J, Szabo A, Skulachev VP, Bauer M, Bahrami S, Weis S, Kozlov AV, Osuchowski MF. Mitochondria-Targeted Antioxidants SkQ1 and MitoTEMPO Failed to Exert a Long-Term Beneficial Effect in Murine Polymicrobial Sepsis. Oxidative Medicine and Cellular Longevity 2017 · PMID 29104729
- Zernii EY, Gancharova OS, Tiulina VV, Zamyatnin AA Jr, Philippov PP, Baksheeva VE, Senin II. Mitochondria-targeted antioxidant SKQ1 protects cornea from oxidative damage induced by ultraviolet irradiation and mechanical injury. BMC Ophthalmology 2018 · PMID 30587174
- Suarez-Rivero JM, Pastor-Maldonado CJ, Povea-Cabello S, Alvarez-Cordoba M, Villalon-Garcia I, Munuera-Cabeza M, Suarez-Carrillo A, Talaveron-Rey M, Sanchez-Alcazar JA. Coenzyme Q10 Analogues: Benefits and Challenges for Therapeutics. Antioxidants (Basel) 2021 · PMID 33557229
- Yuan P, Feng Z, Yang H, Xue H, Xie H, Dai Z, Wang H, Liu Y, Pan B, Song H, Ye H, Xie Z, Shi P, Sun X. Visomitin Attenuates Pathological Bone Loss by Reprogramming Osteoclast Metabolism via the STAT3/LDHB Axis. Research (Washington DC) 2025 · PMID 40698330
- Ji MH, Kreymerman A, Belle K, Ghiam BK, Muscat SP, Mahajan VB, Enns GM, Mercola M, Wood EH. The Present and Future of Mitochondrial-Based Therapeutics for Eye Disease. Translational Vision Science and Technology 2021 · PMID 34232272
- Valdes-Arias D, Locatelli EVT, Sepulveda-Beltran PA, Mangwani-Mordani S, Navia JC, Galor A. Recent United States Developments in the Pharmacological Treatment of Dry Eye Disease. Drugs 2024 · PMID 38652355
Visomitin — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These act on mitochondrial function, NAD+ availability, sirtuin signaling or cellular clearance. The honest prediction is that acute harm is unlikely and the interesting risks are theoretical and long-range — which is a different shape of risk, not an absence of one.
- Growth and clearance signals cut both ways. Anything that improves the efficiency of cell survival is also improving it for cells you would rather not keep. Anything that pushes clearance hard is doing so indiscriminately.
- The near-term, practical ones: NAD+ precursors and infusions commonly cause flushing and a strong sensation if pushed fast, and several compounds in this class are stimulating enough to disrupt sleep.
What has actually been reported
- Generally well tolerated at studied doses. NAD+ infusion discomfort is rate-dependent and resolves by slowing down.
- The human evidence is mostly short trials with surrogate endpoints — a marker moved, not a life changed. That is worth knowing before you build a decade-long habit on it.
How to reduce the risk
Same mechanism as the prediction.
- Slow the infusion rate. Almost all NAD+ discomfort is rate, not dose. There is no prize for finishing quickly.
- Dose earlier in the day. Several of these are subtly stimulating, and sleep is where most of the repair you are paying for happens.
- Pick an endpoint you can actually measure, and take the baseline before you start. This is the class most prone to spending years on something with no way of knowing whether it did anything.
- Fix the basics first. Sleep, training and bloodwork move the same markers further than anything on this list, and they are free. A longevity compound stacked on four hours of sleep is a rounding error.
What it does to your bloodwork
A fact about the assay.
- There is no NAD+ assay worth ordering clinically. Judge this class on downstream markers — inflammatory markers, lipids, fasting glucose, and whatever your baseline panel showed as out of range.
Don't run this if
- Active malignancy, for the survival-signaling reasoning above.
- Pregnancy — uncharacterized.
The honest unknown
- Whether any of it extends healthspan in humans. Every honest person in this field is running on mechanism and animal data, and this catalog should say so rather than imply otherwise.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Visomitin — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Visomitin moves on your bloodwork
Expected direction, not a measured one.
- hs-CRP (High-Sensitivity C-Reactive Protein) — ↓ expected to fall
Where these work, systemic inflammation is the plausible readout.
What to do: hs-CRP is cheap and moves. Baseline and 12 weeks. - HbA1c (Hemoglobin A1c) — ↓ expected to fall
Improved mitochondrial and metabolic function should show here if the effect is real at all.
What to do: The honest use of these markers is as a falsification test: if nothing moves in 12 weeks, the compound is not doing much for you. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
Liver and kidney function — the standard baseline for anything run long term.
What to do: Twice a year is enough on a stable protocol.
This class is where honest expectation-setting matters most: the markers above are how you find out whether anything happened, and for most of these compounds that question is genuinely open.
- Dose range and how to work up to it
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Visomitin in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Visomitin
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Visomitin — frequently asked questions
What is Visomitin?
Visomitin (SkQ1, Skulachev ions, plastoquinonyl decyltriphenylphosphonium, MitoVitan, MitoVitan Active, Exomitin, the same active in an eye drop and in three topicals) is a longevity & bioregulators research compound. A plastoquinone head group tethered by a ten-carbon chain to a triphenylphosphonium cation. The cation is the delivery mechanism and it is the whole idea: a lipophilic positive charge is driven across membranes by the electrical potential they carry, and the mitochondrial inner membrane carries the largest potential in the cell, so the molecule accumulates there by electrophoresis rather than by any receptor. The plastoquinone then does what it does in a chloroplast — intercepts the lipid peroxidation chain in the membrane it is sitting in. Concentration is the whole safety argument, because the same charge that concentrates it will uncouple respiration if there is too much of it.
Where can I find Visomitin dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Visomitin protocol are available to members inside Skool. This public page covers what Visomitin is, how it works and the evidence.
What is the half-life of Visomitin?
Visomitin has an approximate half-life of Not characterized in humans for the ophthalmic product, which is part of what determines how often it's dosed.
What's the evidence behind Visomitin?
Current evidence level: Registered in Russia as an eye drop — the only registered SkQ1 medicine anywhere. One published phase 2 trial in dry eye. Not FDA-approved.. Visomitin is offered for research purposes only and is not an approved medicine.
What Visomitin is used for
Visomitin appears under 1 goal in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.