Crystagen
BioregulatorsResearch Use OnlyLast reviewed: September 28, 2026
Quick Facts
- What it is
- A synthetic short peptide from the Khavinson bioregulator programme, studied for immune effects. Its amino-acid sequence could not be sourced to any primary publication.
- How it's taken
- Not established — the single study located is laboratory work on spleen tissue and reports no human route
- Half-life
- Not characterized
- Typical research dose
- No validated dose — no human regimen appears in any source located
- Research status
- Not FDA- or EMA-approved — US research use only. One indexed paper names it, in Russian, from the originating institute; zero registered trials.
On this page
Where to source Crystagen
Crystagen is not approved for human use and is sold by specialty research peptide vendors for laboratory use only. The bioregulator line is more specialised than the mainstream catalog, so fewer vendors carry it — Prof. Peptide's price data currently tracks one vendor for this compound. One caveat is specific to Crystagen: with no sourceable amino-acid sequence, a Certificate of Analysis here asserts an identity a buyer cannot check against an independent primary reference.
Per-batch COAs
What is Crystagen?
Crystagen is one of the synthetic short peptides from the Khavinson bioregulator programme, developed at the Saint-Petersburg Institute of Bioregulation and Gerontology and studied for effects on the immune system. It sits alongside siblings such as Thymogen, Cartalax and Cardiogen; the bioregulator guide sets out how the family is organised and where the extracts and the synthetics differ.
This is the thinnest evidence base of any compound in this library. PubMed holds exactly one record that names Crystagen. It is in Russian, from the institute that developed the compound, and it has never been replicated. Prof. Peptide could not even locate a primary source stating the compound's amino-acid sequence — secondary sites give one, but none that could be checked. The page is short because the record is, and padding it would misrepresent how much is actually known. New to peptide research? Start with the basics
Reported in the cited work: activation of the B-cell arm of the immune system in the ageing spleen, and — stated in the same paper — no effect on cell renewal in the spleen as it ages, unlike the three peptides it was compared against [1]. A separate paper from the same programme proposes that short peptides act by binding DNA directly, modelled by molecular docking, but it does not name Crystagen [2].
How is Crystagen proposed to work?
There is a family-level mechanistic proposal and there is a compound-level finding, and they are not the same strength of claim. Both are reported below with their provenance attached.
- The compound-level finding [1]. In the ageing spleen, Crystagen was reported to activate the B-cell arm of the immune system. The same paper reports that it did not affect cell renewal in the spleen with age — the effect ascribed to it is narrower than those ascribed to the three peptides it was compared against (Chervyakova et al. 2014).
- The family-level proposal, which does not name this compound [2]. The programme's general hypothesis is that short peptides cross the cytoplasmic and nuclear membranes and bind DNA directly, one peptide regulating dozens of genes. Spatial DNA-peptide models were built for 19 short peptides by molecular docking (Khavinson et al. 2016). Docking is a computational model rather than a measurement, the paper states it as a supposition, and Crystagen is not among the peptides it names.
- The sequence could not be sourced. Prof. Peptide found no indexed publication giving Crystagen's amino-acid sequence. Vendor listings and secondary sites state one; none that could be checked against a primary source. It is left unstated here rather than repeated, because a sequence is exactly the kind of fact that looks authoritative once written down.
- No binding target, no pharmacokinetics, no dose-response. None of these appears in the literature located for this compound.
What is Crystagen researched for?
This is the shortest research section on the site, and the length is the finding. What follows is the complete indexed record for this compound, not a selection from it.
- Immune activity in the ageing spleen, one study [1]. B-cell activation reported; cell renewal in the ageing spleen explicitly not affected. Compared against Vilon, Timogen and R-1 in the same experiment (Chervyakova et al. 2014).
- That is the entire indexed literature. A PubMed search for "Crystagen" returns one record. Searching the title-and-abstract field returns the same one. No second study, no replication, no review devoted to it.
- Nothing in the trial registries. ClinicalTrials.gov returns zero registered studies for Crystagen. The same query returns 788 for semaglutide, so the probe works and the zero is about this compound.
- No sourceable sequence. Unusually even for this family, Prof. Peptide could not find a primary source stating which amino acids Crystagen is made of.
How is Crystagen dosed, and what is known about safety?
Both answers are the same answer, which is why they sit in one section: there is no published human work on this compound, so there is neither a dose to report nor a safety record to summarise.
The single study located is laboratory work on spleen tissue and states no human regimen [1]. No clinical study of any design was found, and no trial is registered. Prof. Peptide therefore publishes no milligram figure, no schedule and no route for Crystagen — not as caution, but because no source exists to report one from. On safety, the position needs saying plainly rather than left as an omission: there is no adverse-event data for Crystagen in humans, no interaction data, and no long-term follow-up, because no person has been studied taking it in any report located here. An absence of reported harm in one laboratory paper is not a safety record, and it should not be read as one. The uncertainty extends past the biology to the vial: with no sourceable sequence, a Certificate of Analysis for Crystagen is an identity claim a buyer cannot check against an independent primary reference. That is a narrower guarantee than a COA gives for a compound whose sequence is published.
What are the limitations of Crystagen research?
One paper. That is the whole of it. It is in Russian with an English abstract indexed, it comes from the Saint-Petersburg Institute of Bioregulation and Gerontology — the institute that originated the bioregulator programme — and it has not been replicated by anyone, anywhere.
Within that paper, Crystagen is not the strongest performer. It is one of four peptides compared, and the reported result for it is B-cell activation without the cell-renewal effect the others showed. A profile that quoted only the activation half would be reporting a selection rather than the finding.
The mechanism usually attached to this compound belongs to the family, not to it. The DNA-binding account comes from a molecular-docking paper that does not name Crystagen, and docking produces a model rather than a measurement.
No human data, no registered trial, no FDA or EMA approval, and no sourceable amino-acid sequence. Crystagen is research-use-only material. The same caveats apply across this family — see the bioregulator guide , and Cartalax for a sibling compound with the same single-institute problem and slightly more literature behind it.
Crystagen FAQ
What is Crystagen?
Crystagen is one of the synthetic short peptides from the Khavinson bioregulator programme, studied for effects on the immune system. Beyond that, this profile can say less than most: PubMed holds exactly one record that names Crystagen, it is in Russian, and Prof. Peptide could not locate a source giving the compound's amino-acid sequence. The bioregulator guide explains how this family is organised.
Is Crystagen FDA-approved?
No. Crystagen is not approved by the FDA or the EMA for any indication, and Prof. Peptide located no registration for it outside the Russian Federation. It is sold as research-use-only material. A ClinicalTrials.gov search returns zero registered studies, against 788 for semaglutide on the same query, so the zero is a finding and not a broken search.
What does the one study on Crystagen actually say?
It compared four short peptides — Vilon, Timogen, Crystagen and R-1 — for immunoprotective effects in the ageing spleen. Crystagen was reported to activate the B-cell arm of the immune system. The same sentence reports what it did not do: unlike the others, Crystagen did not affect cell renewal in the ageing spleen. The other three each had a mechanism attached — Vilon and R-1 activating T-helpers, Timogen activating B-cells through reduced apoptosis and increased proliferation. Crystagen is the one in that comparison with the narrowest reported effect.
Why is there so little to read about Crystagen?
Because one indexed paper is all there is. That paper is in Russian with only an English abstract indexed, and it comes from the Saint-Petersburg Institute of Bioregulation and Gerontology — the institute that originated the bioregulator programme. There is no independent group, no English-language primary literature, and no second study to check the first against. This is the same pattern that runs through the whole family, in its most extreme form.
Is there a standard Crystagen dose?
No. No validated dose exists. The single study located is laboratory work on spleen tissue and reports no human regimen, and Prof. Peptide found no clinical study of any design. No milligram figure, schedule or route is published here, because there is no source to report one from.
References
- Chervyakova NA, Linkova NS, Chalisova NI, Koncevaya EA, Trofimova SV, Khavinson VK. [Molecular aspects of immunoprotective activity of peptides in spleen during the ageing process]. Adv Gerontol. 2014;27(1):224-228. [Article in Russian; English abstract.] PMID 28976144. https://pubmed.ncbi.nlm.nih.gov/28976144/
- Khavinson VK, Lin'kova NS, Tarnovskaya SI. Short peptides regulate gene expression. Bull Exp Biol Med. 2016;162(2):288-292. doi:10.1007/s10517-016-3596-7. PMID 27909961. Cited for the programme's general mechanism only — this paper does not name Crystagen. https://pubmed.ncbi.nlm.nih.gov/27909961/
Published Studies
Plain-English summaries of the two indexed papers behind the statements above. Click either title to read the source record. Only the first names Crystagen; the second is included so the family-level mechanism can be read for what it is.
Chervyakova NA, Linkova NS, Chalisova NI, Koncevaya EA, Trofimova SV, Khavinson VK.
The only PubMed record that names Crystagen. Four short peptides — Vilon, Timogen, Crystagen and R-1 — were compared for immunoprotective effects in the ageing spleen. Vilon and R-1 were reported to activate T-helpers, Vilon through reduced apoptosis and R-1 through increased proliferation and differentiation; Timogen activated B-cells by reducing apoptosis and increasing spleen-cell proliferation. Crystagen also activated the B-cell arm, but the paper states it did not cause cell renewal in the spleen as it ages. The indexed abstract does not state whether the spleen tissue was cultured or studied in living animals, so the design cannot be pinned down from what is readable. Russian-language, from the Saint-Petersburg Institute of Bioregulation and Gerontology.
Khavinson VK, Lin'kova NS, Tarnovskaya SI.
Listed for context, and it does NOT name Crystagen. This is the programme's general mechanistic proposal: that short peptides penetrate the cytoplasmic and nuclear membranes and bind DNA directly, one peptide regulating dozens of genes. Spatial models of DNA-peptide complexes were constructed for 19 short peptides by molecular docking, with peptides KE and EDP binding an agat sequence, KEDW and AED an acct sequence, and AEDL and EDL a ctcc sequence. Two things to hold onto: docking is a computational model, not a measurement, and the paper's own framing is "we suppose that" — an explicitly stated hypothesis. It is cited here to show what mechanism this family proposes in general, not as evidence about this compound.
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