Trekrezan
Crezacine — tris(2-hydroxyethyl)ammonium methylphenoxyacetate, a protatrane
Trekrezan (Crezacine — tris(2-hydroxyethyl)ammonium methylphenoxyacetate, a protatrane) is a healing & recovery research compound. An ammonium salt pairing a tri-hydroxyethyl cation with a substituted phenoxyacetic acid anion, belonging to the protatranes — the proton-centered members of the atrane family developed at Irkutsk by Voronkov's school. It contains no silicon, despite frequently being described in the market as an organosilicon agent. The published immunology is bidirectional in the same abstract: decreased spot-forming activity of polypotent stem blood cells alongside stimulated lympho- and hemopoiesis, antibody formation and direct stimulation of human B lymphocyte proliferation in vitro.
Trekrezan quick facts
| Route | Oral |
| Frequency | Not established · Not established |
| Half-life | Unpublished. An ionic pair separates on dissolution, and nobody has established which species circulates |
| Forms | Oral |
| Evidence level | Four studies, all from one school, all in mice or cells. No controlled human trial exists. |
Every published study of this compound over thirty-three years carries an author from the same institution, and there is no human trial of any kind — the ladder runs from human cells in a dish to mouse pups and stops. The name also changed: the same molecule was published as crezacine, and searching one spelling finds half the record. The specific claim worth testing is the 1993 in vitro finding of direct B lymphocyte stimulation, which predicts a measurable shift on a standard lymphocyte panel. Nobody has drawn one. And if that claim is right, the people it is least suited to are those with antibody-mediated autoimmune disease — which no vendor mentions.
How Trekrezan works
An ammonium salt pairing a tri-hydroxyethyl cation with a substituted phenoxyacetic acid anion, belonging to the protatranes — the proton-centered members of the atrane family developed at Irkutsk by Voronkov's school. It contains no silicon, despite frequently being described in the market as an organosilicon agent. The published immunology is bidirectional in the same abstract: decreased spot-forming activity of polypotent stem blood cells alongside stimulated lympho- and hemopoiesis, antibody formation and direct stimulation of human B lymphocyte proliferation in vitro.
Proposed benefits
Researched for soft-tissue and gut repair, reduced inflammation, angiogenesis and faster recovery from injury.
Where to get Trekrezan
Buy Trekrezan at RUPharma →The evidence for Trekrezan
Graded by what exists behind each claim.
✅ Clinically validated
- There is no controlled human trial of this compound. Not a trial, not a case series, not a tolerability report. A PubTator3 search on 9 September 2026 returns 24 records of which four are on topic, and every one of them is in mice or in cells.
📊 Correlative data
- Every published study across thirty-three years carries an author from one institution. Voronkov appears on the 2003, 2004 and 2010 papers and on the 1993 immunology work with the Novosibirsk group, and the 2021 chemistry review is explicitly an account of that school's contribution (Kondratenko 2021). Independent replication is how a finding stops being one laboratory's opinion, and it has not happened.
- The name changed and the older one finds different papers. The same molecule was published as crezacine — a 1985 study of exocrine pancreatic activity and a 2000 paper on microbiological synthesis — neither of which the current brand name retrieves.
🧪 Theoretical / extrapolated
- An ammonium salt pairing a tri-hydroxyethyl cation with a substituted phenoxyacetic acid anion, belonging to the protatranes, the proton-centered members of the atrane family. It contains no silicon, despite the market describing it as organosilicon.
- The 1993 work reports decreased spot-forming activity of polypotent stem blood cells alongside stimulated lympho- and hemopoiesis, antibody formation, steady anti-inflammatory activity, and direct stimulation of human B lymphocyte proliferation in vitro (Shirinskii 1993). A claim that a substance raises what is low and lowers what is high cannot be falsified by any single measurement.
- Predicted downside from its own efficacy claim: if it really stimulates antibody production (Voronkov 2004), the people it suits least are those with antibody-mediated autoimmune disease and those on transplant immunosuppression. Neither group has been studied and no vendor names them.
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 Trekrezan actually does
The chemistry is a family most readers have never heard of, and naming it correctly is the start. Trekrezan is tris(2-hydroxyethyl)ammonium methylphenoxyacetate — an ammonium salt pairing a tri-hydroxyethyl cation with a substituted phenoxyacetic acid anion. It belongs to the protatranes, the proton-centered members of the atrane family developed at Irkutsk by the school of Mikhail Voronkov, whose chemistry Kondratenko 2021 reviews. The better-known members of that family are the silatranes, where a silicon sits at the center of the same cage. This one has no metal in it at all, which is worth stating because the compound is often described in the market as an organosilicon agent.
The claimed mechanism is immunomodulation, and the word is doing a lot of work. Shirinskii 1993 reports that in vivo the compound decreased the spot-forming activity of polypotent stem blood cells while stimulating lympho- and hemopoiesis, antibody formation and showing steady anti-inflammatory activity, and that in vitro it stimulated human mononuclear cell proliferation through direct action on B lymphocytes with increased lymphokine and monokine production. Notice the shape of that: one compartment suppressed, several stimulated, in the same abstract. A claim that a substance raises what is low and lowers what is high cannot be falsified by any single measurement, and that is a property of the claim rather than of the immune system.
The second published action is vascular and much thinner. Voronkov 2010 reports an antisclerotic effect and proposes mechanisms. It is a short communication in a proceedings journal, from the same laboratory, and it is the only cardiovascular claim in the compound's entire record.
How it is sold, and against what. A partner lists it at $31 as an adaptogen and immunomodulator. That word places it beside a category with its own literature and its own definitional problems Todorova 2021 — and the plant adaptogens at least have controlled human trials to argue about. This one does not.
Cell, rodent, human — and where it stops
Every published study of this compound comes from one school, and that is checkable from the author lists. Voronkov MG appears on Voronkov 2004, Kolesnikova 2003 and Voronkov 2010, and on Shirinskii 1993 alongside the Novosibirsk immunology group; the 2021 chemistry review Kondratenko 2021 is explicitly an account of that school's contribution. Independent replication is the ordinary way a finding stops being one laboratory's opinion, and for this compound it has not happened in more than thirty years.
The species ladder stops before it reaches a person. Shirinskii 1993 is animal work plus human cells in a dish. Voronkov 2004 studied mouse pups after vaccinating adult mice during pregnancy and after vaccinating the pups at various ages, and reports that the preparation modulated immune activity and stimulated antibody production pre- and postnatally. Kolesnikova 2003 describes it as a modulator of hemato- and immunopoiesis. There is no controlled human trial of this compound in the searchable literature, and a PubTator3 query on 9 September 2026 for the product name returned 24 records of which the on-topic ones are the four cited here.
The name changed, and the older name finds different records. The same molecule was published as crezacine — the 9 September 2026 search returns a 1985 study of its effect on exocrine pancreatic activity (PMID 2415314) and a 2000 paper describing crezacin as a biostimulator for microbiological synthesis (PMID 10687052), neither of which is retrieved by searching the current brand name. Naming both spellings is deliberate: a reader who searches one word and finds four papers has not found the literature.
And the one place where the record is genuinely interesting. The 1993 in vitro finding is specific rather than vague — direct stimulation of B lymphocyte proliferation with increased cytokine output Shirinskii 1993. That is a measurable prediction about a human immune parameter, made 33 years ago, in human cells. It has never been followed into a person, which is the gap this page is actually about.
Trekrezan pharmacokinetics — how much of it actually gets in
No pharmacokinetic study of this compound has been published. No oral bioavailability, no time to peak, no half-life, no clearance route, no analyte defined for measuring it in plasma. None of the four studies above reports a concentration Shirinskii 1993 Kolesnikova 2003 Voronkov 2004 Voronkov 2010. That is the starting position and everything below is reasoning from chemistry rather than from measurement.
What the salt form implies, and it is unusually predictable. This is an ionic pair: a permanently charged quaternary-like ammonium cation and a phenoxyacetate anion. In solution the pair dissociates, so the two halves are absorbed separately and the compound does not travel as a unit. Phenoxyacetic acids are small, acidic, well absorbed from the small intestine, extensively bound to albumin and cleared renally with active tubular secretion — that is the general behavior of the class. The tris(2-hydroxyethyl)ammonium cation is small, highly polar and renally cleared. Neither half has a reason to persist.
Which produces a specific and awkward question. If the pair separates on dissolution, then whatever the atrane cage contributes to the biology has to survive that separation, and the family's own chemistry review Kondratenko 2021 is about compounds whose interest lies in the intact cage. Nobody has published whether the administered species and the circulating species are the same thing. For an ionic pair given orally, that is the first experiment, and it is missing.
The dosing consequence. With no half-life there is no basis for a schedule, and with no analyte there is no way to check adherence, accumulation or a missed dose. The vendor's stated regimen is therefore a convention rather than a derivation, and this page states no dose.
What would have to be true, and how you would know it was not
Three predictions, and the first is the one the 1993 paper set up and nobody collected.
1. A lymphocyte subset panel before and after a course. Total white cell count, absolute lymphocytes, and CD4/CD8 with B-cell and NK subsets. The in vitro result was direct stimulation of B lymphocyte proliferation with increased cytokine production Shirinskii 1993, which predicts a measurable shift in the B cell compartment. The panel is standard, it is available in most labs, and no published study of this compound reports it in a person.
2. Immunoglobulin G, and the vaccine test that would settle it. The animal work is about antibody formation after vaccination Voronkov 2004. The human version is not complicated: take the compound across a routine vaccination and measure the antibody titer response against unexposed controls. That single experiment would move this product from mouse pups to people, and it is the most obvious study nobody has run.
3. Against the product, and it is the falsification the claim resists. An immunomodulator that both raises and lowers is not testable. The falsifiable version is directional: predict that hs-CRP is unchanged and that the lymphocyte panel above is unchanged after a full course in a healthy adult. If those hold, the in vitro B cell result did not transfer to a swallowed dose, which is the outcome the absent pharmacokinetics would lead a pharmacologist to expect.
What nobody has tested yet
Nobody outside one school has studied it. Thirty-three years after the first immunology paper Shirinskii 1993, every published study still carries an author from the same institution. That is not evidence the work is wrong. It is the reason no independent reader can tell whether it is right, and it is the single most useful thing to know before buying it.
Nobody has run any human study. Not a trial, not a case series, not a tolerability report. The ladder runs from human cells in a dish Shirinskii 1993 to mice Voronkov 2004 and stops. A twenty-person open tolerability study with a lymphocyte panel would be a week's work and would double what is publicly known about this compound.
Nobody has established what circulates. An ionic pair given orally separates into two ions with different fates, and no analysis identifies which species reaches blood or in what proportion. Until somebody does, the atrane chemistry that makes the compound interesting Kondratenko 2021 cannot be connected to any biological effect observed after swallowing it.
Extrapolation, labeled as such. If the compound really acts on B lymphocytes as the 1993 in vitro work reports, three consequences follow that have never been looked for: the effect should be visible as an improved antibody response to a vaccine given during a course; it should be larger in people whose baseline immunoglobulin is low; and it should be a reason for caution rather than enthusiasm in anybody with an autoimmune condition, where stimulating antibody production is not a benefit. The third of those is a safety implication of the product's own efficacy claim, and no vendor states it.
Trekrezan — its own safety story, not its class's
Three things specific to this compound.
An immune stimulant has a population it should not be sold to, and the marketing does not name one. The published claim is stimulation of antibody formation and B lymphocyte proliferation Shirinskii 1993 Voronkov 2004. If that is real, then the people for whom it is least appropriate are those with antibody-mediated autoimmune disease and those on immunosuppression after a transplant — the two groups where deliberately pushing the antibody arm is the opposite of the treatment plan. No study has examined either group and no product page names them.
There is no adverse event record because there is no human study. Zero reported side effects, from zero published trials in people. That is a statement about the literature and not about the compound, and treating it as reassurance is the specific error this page exists to prevent. The animal work is short-term; nothing addresses chronic exposure in a person at any dose.
And the anti-inflammatory claim is the one that could mask something. Shirinskii 1993 reports steady anti-inflammatory activity. Anything that blunts an inflammatory response also blunts the signal a person uses to notice an infection or an injury getting worse. That is a general property of anti-inflammatory agents rather than a peculiarity of this one, and for a compound with no human dose-response it is the mechanism most likely to matter first.
Sources read for this page
- Shirinskii VS, Kolesnikova OP, Kudaeva OT, et al. [The immunoactive properties of trekrezan]. Eksperimentalnaia i Klinicheskaia Farmakologiia 1993 [Russian] · PMID 8219991
- Voronkov MG, Pavel YG, Karus AL, et al. Effect of trekrezan on immunogenesis under experimental conditions. Bulletin of Experimental Biology and Medicine 2004 · PMID 15662463
- Kolesnikova OP, Kudaeva OT, Sukhenko TG, et al. Trekrezan as a modulator of hemato- and immunopoieses. Doklady Biological Sciences 2003 · PMID 14556517
- Voronkov MG, Nurbekov MK, Bobkova SN, et al. Antisclerotic effect of Trekrezan and its possible mechanisms. Doklady Biochemistry and Biophysics 2010 · PMID 20514866
- Kondratenko YA. Contribution of the Scientific School of Academician M.G. Voronkov to the Development of the Chemistry of Biologically Active Atranes (Protatranes and Hydrometallatranes). Russian Journal of General Chemistry 2021 · PMID 35068915
- Todorova V. Plant Adaptogens - History and Future Perspectives. Nutrients 2021 · PMID 34445021
Trekrezan — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Trekrezan moves on your bloodwork
Expected direction, not a measured one.
- Complete Blood Count (CBC) with Differential — ◆ worth watching
A complete blood count with differential is the measurement this compound's own literature predicts. The 1993 work reports stimulated lympho- and hemopoiesis and direct stimulation of B lymphocyte proliferation in human cells; the 2003 paper describes it as a modulator of hemato- and immunopoiesis. If any of that transfers to a swallowed dose, the lymphocyte line is where it would appear.
What to do: Baseline before a course and again at the end. Nothing published reports this measurement in a person taking it, so a reader who runs it knows something the literature does not. - hs-CRP (High-Sensitivity C-Reactive Protein) — ◆ worth watching
The same 1993 paper reports steady anti-inflammatory activity. That is a directional claim and hs-CRP is the cheap standardized way to test it.
What to do: Draw it with the blood count rather than separately, and not within two weeks of an infection or a hard training block. - Comprehensive Metabolic Panel (CMP) — ◆ worth watching
The general baseline for a compound with no published human pharmacokinetics, not a targeted test.
What to do: Baseline, and again on any extended run.
Every published study of this compound comes from one school and none of them is in a human being. Four papers across thirty-three years, all carrying an author from the same institution, all in mice or in cells. There is no human interaction data because there is no human data.
- 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 — Trekrezan in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Trekrezan
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Baseline inflammation — the thing you're claiming to reduce |
| Complete Blood Count (CBC) with Differential | Infection, anemia and platelet count before anything injectable |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney baseline |
| Vitamin D (25-Hydroxy) | Low D slows soft-tissue and bone healing measurably |
The Inflammation Deep Dive panel covers these in one order — 10 markers, $248.35 with the discount applied.
Check results you already have → · All 103 markers A–Z
Trekrezan — frequently asked questions
What is Trekrezan?
Trekrezan (Crezacine — tris(2-hydroxyethyl)ammonium methylphenoxyacetate, a protatrane) is a healing & recovery research compound. An ammonium salt pairing a tri-hydroxyethyl cation with a substituted phenoxyacetic acid anion, belonging to the protatranes — the proton-centered members of the atrane family developed at Irkutsk by Voronkov's school. It contains no silicon, despite frequently being described in the market as an organosilicon agent. The published immunology is bidirectional in the same abstract: decreased spot-forming activity of polypotent stem blood cells alongside stimulated lympho- and hemopoiesis, antibody formation and direct stimulation of human B lymphocyte proliferation in vitro.
Where can I find Trekrezan dosing and protocols?
Dosing, the reconstitution calculator and Coach Cam's full Trekrezan protocol are available to members inside Skool. This public page covers what Trekrezan is, how it works and the evidence.
What is the half-life of Trekrezan?
Trekrezan has an approximate half-life of Unpublished. An ionic pair separates on dissolution, and nobody has established which species circulates, which is part of what determines how often it's dosed.
What's the evidence behind Trekrezan?
Current evidence level: Four studies, all from one school, all in mice or cells. No controlled human trial exists.. Trekrezan is offered for research purposes only and is not an approved medicine.
What Trekrezan is used for
Trekrezan appears under 1 goal in the goal router.
Related Healing & Recovery 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.