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Cardiogen4 residuesAEDREach bubble = one amino acid. Size = residue mass. Color = chemical class.Also known as: AEDR, Cardiogen peptide, Cytogen Cardiogen
Four amino acids. That's all Cardiogen is. Ala-Glu-Asp-Arg, a synthetic tetrapeptide from Vladimir Khavinson's bioregulator program at the St. Petersburg Institute of Bioregulation and Gerontology. In organotypic rat cardiac tissue cultures, picomolar concentrations of this sequence triggered cardiomyocyte proliferation that none of the 20 individual amino acids could reproduce [1]. That finding is genuinely interesting. It's also the full extent of the evidence. Zero human trials exist. Zero Western labs have replicated the work. No pharmacokinetic data of any kind has been published. Cardiogen occupies a niche used almost exclusively by Khavinson protocol followers running multi-organ bioregulator stacks alongside Epithalon and Thymalin.
Cardiogen (Ala-Glu-Asp-Arg, CAS number not publicly assigned) is a synthetic tetrapeptide bioregulator from the Khavinson "cytogen" class, designed to target cardiac tissue gene expression. At picomolar concentrations, it stimulated cardiomyocyte proliferation in organotypic cultures from aged rats [1]. None of the 20 individual L-amino acids tested at identical concentrations produced the same effect. The intact four-residue sequence appears to be required. Cardiogen belongs to a family of short peptides proposed to cross cell membranes without receptor-mediated transport and bind histone proteins in the nucleus. These short peptides are proposed to cross cell membranes without receptor-mediated transport and bind histone proteins in the nucleus. The downstream theory: altered chromatin conformation opens cardiac-specific gene promoter regions, upregulating structural proteins like myosin heavy chain and troponin I. Two formulations circulate. The original Russian Cytogen brand sells oral capsules (2 caps, 1 to 2 times daily for 30 days). Western research vendors offer 20 mg lyophilized vials for subcutaneous injection at 10 to 20 mg per day over 10 to 20 days. Oral bioavailability is unknown and probably low; GI proteolysis breaks down tetrapeptides quickly. The community footprint is nearly invisible. Fewer than 20 English-language experience reports exist across all forums. Reddit's r/peptides and r/nootropics have zero dedicated threads. LongeCity bioregulator discussions mention Cardiogen as part of multi-organ stacks, never in isolation. All published data comes from a single Russian research group and its affiliates. A 2022 review in Cells [2] positioned AEDR as a SASP modulator in cardiovascular inflammaging but added no new experimental data. The honest assessment: plausible preclinical mechanism, zero human validation.
Khavinson's bioregulation model proposes something unusual. Short peptides like Cardiogen don't bind cell-surface receptors. They're small enough to pass through membranes and enter the nucleus directly, where they reportedly bind histone proteins H1, H2b, H3, and H4. That histone binding alters chromatin conformation. Tightly packed DNA becomes more accessible at cardiac-specific promoter regions. The result, at least in tissue culture, is upregulation of genes encoding myosin heavy chain, troponin I, and titin (cardiac structural proteins). PGC-1alpha and TFAM (mitochondrial biogenesis regulators) and the anti-apoptotic factors Bcl-2 and Akt also increase. The p53 connection matters. Immunohistochemical analysis showed reduced p53 protein expression in treated myocardial tissue [1]. p53 drives apoptosis; suppressing it shifts cardiomyocytes toward survival and proliferation. In aged rat cardiac tissue cultures, AEDR at picomolar concentrations produced both increased proliferation and decreased apoptosis simultaneously. One detail stands out. Twenty individual L-amino acids were tested at the same concentration. None reproduced the effect. The intact tetrapeptide sequence appears required for bioactivity, suggesting the mechanism depends on the specific AEDR conformation interacting with DNA or histones. This entire model remains unconfirmed outside Khavinson's group. No independent Western lab has replicated any of these findings in any system. No direct DNA-binding assay data for AEDR has been published.
Preclinical data only from a single Russian research group. Cardiogen (AEDR) stimulates cardiomyocyte proliferation and suppresses p53-mediated apoptosis in organotypic tissue cultures from aged rats: uniquely at picomolar concentrations that failed to reproduce with individual amino acids. A 2022 Khavinson review (Cells)[2] identifies AEDR as a candidate modulator of SASP (senescence-associated secretory phenotype) in cardiovascular inflammaging. No independent Western replication. No human trials. No human PK data.
Khavinson et al. (2009) PMID 20210190: "The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats." Primary study establishing picomolar cardiomyocyte proliferation effect and p53 suppression. All data from organotypic rat cardiac tissue cultures.
All published data from one lab and its affiliates. No independent Western replication in any model system. No human trials of any design. No pharmacokinetic data (half-life is class-estimated, not measured). Oral bioavailability unknown, likely low due to GI proteolysis. Commercial capsule per-dose peptide content not publicly disclosed. The 2022 review (PMID 36611900) is theoretical positioning, not new experimental data.
Virtually no independent Western community presence. No dedicated threads found on r/peptides or r/nootropics as of 2026. Used almost exclusively within Khavinson full-organ bioregulator stacks discussed on LongeCity, not as a standalone peptide. The few reporters are describing stack-level outcomes, not Cardiogen-specific effects.
Preclinical science establishes a plausible cardiac-specific mechanism. Community use is too limited to independently confirm or contradict any effect. Alignment cannot be meaningfully assessed: the community dataset is essentially empty. Any community claims derive directly from the same Khavinson publications that constitute the scientific evidence base, not from independent user experience.
| Level | Dose / Injection | Frequency |
|---|---|---|
| Beginner | 10mg | Daily |
| Moderate | 20mg | Daily |
| Aggressive | 20mg | 2x Daily |
Cardiogen comes in two forms and the protocols are not interchangeable. The Russian Cytogen capsules follow the label: 2 caps, once or twice daily, 30 days. The Western injectable vials (20 mg lyophilized) use subcutaneous injection at 10 to 20 mg per day for 10 to 20 days. For injectable reconstitution: add 2 mL bacteriostatic water to a 20 mg vial. That gives you 10 mg per mL. A 10 mg dose is 1.0 mL, which is 100 units on a U-100 insulin syringe. One vial gives you exactly 2 doses at 10 mg per day, or 1 dose at 20 mg per day. You won't feel anything. That's normal. The proposed mechanism is cardiomyocyte gene expression modulation, not something that produces a perceivable sensation. Absence of subjective effect does not mean the product failed or worked. Verify your vial with a COA showing HPLC purity at or above 98% and mass spectrometry confirming molecular weight around 489.5 Da for AEDR.
Standard Khavinson bioregulator protocol: 1-2 capsules daily for 10-20 consecutive days, repeated every 3-6 months. Courses are often combined with other organ-specific bioregulators.
Khavinson bioregulator cycling is based on epigenetic persistence theory, not receptor desensitization or hormone axis recovery. Short courses are proposed to trigger cellular gene expression changes that stabilize and persist for months after the peptide is cleared. Continuous administration is considered unnecessary: the goal is initiating a regulatory process, not maintaining a blood level. The 3-6 month off-period also reflects the complete absence of long-term human safety data, making extended breaks a precautionary default.
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Expected: No validated human outcomes. Proposed mechanism: cardiomyocyte gene expression normalization. Not expected to produce perceivable subjective effects that distinguish from placebo. Any benefit would be cellular-level and cumulative across multiple courses.
Monitor: No validated biomarker for Cardiogen response. Routine annual cardiovascular labs (lipid panel, BNP, EKG) are reasonable for anyone running longevity protocols but are not expected to change from a short course.
Take 2 capsules with a small glass of water, 15 to 20 minutes before a meal. Morning is preferred. 2. Swallow whole. Do not chew or open the capsule. 3. Repeat daily for 30 consecutive days. 4. After the 30-day course, stop for 3 to 6 months before the next course. 5. Most users run 2 courses per year.
Swirl gently; do not shake. Solution must be clear and colorless. 2. This creates a 10 mg per mL concentration. 3. For a 10 mg dose: draw 100 units (1.0 mL) on a U-100 insulin syringe. One vial provides 2 doses. 4. For a 20 mg dose: draw the full 200 units (2.0 mL). One vial provides 1 dose. 5. Use a 29 to 31 gauge insulin syringe. Inject subcutaneously into the abdomen or thigh. Rotate sites. 6. Administer once daily, morning or before bed. 7. Run for 10 to 20 days, then stop for 3 to 6 months. 8. Store reconstituted solution refrigerated at 2 to 8 degrees C. Use within 2 to 3 weeks.
For oral capsules (Cytogen brand):
For injectable (research-grade 20 mg vials):
2 capsules 1-2x/day per official label. Per-capsule peptide content not disclosed. Oral bioavailability of AEDR is unknown: likely low due to GI proteolysis (DPP-4, trypsin). Russian protocol acknowledges this with multi-week courses.
Only route with an established commercial product. Official 30-day course per label. Convenient but uncertain systemic bioavailability. Excipients include lactose: relevant for lactose-intolerant users.
10-20 mg/day SC. No comparative PK data vs oral. Injectable should achieve higher plasma exposure than oral but no bioavailability study confirms this for AEDR specifically.
Western research vendor format (20mg lyophilized vials). No published SC-specific protocol. Reconstitute with 2mL bacteriostatic water for 10mg/mL working solution (100 units on U-100 syringe = 10mg dose). Use 29-31G insulin syringe; rotate sites.
Standard Khavinson multi-bioregulator longevity stack. Epithalon targets pineal/telomere system; Cardiogen targets cardiac tissue. Different organ targets, run concurrently or overlapping in the same cycle period. The most cited Cardiogen stack in bioregulator community discussions.
Epithalon 10mg/day SC for 10 days + Cardiogen 2 caps/day oral for 30 days, overlapping start dates
Khavinson immune + cardiac bioregulator combination. Thymalin targets thymic function and immune aging; Cardiogen targets cardiac tissue. Combined in Khavinson institute multi-organ aging protocols.
Concurrent oral courses per Khavinson full-organ bioregulator protocol schedule
Khavinson brain/neuroendocrine bioregulator. Combined with Cardiogen in users following comprehensive organ-specific bioregulator stacks (cardiac + CNS + immune + endocrine targets simultaneously).
Cardiogen contains arginine, a nitric oxide precursor. ACE inhibitors and ARBs also modulate the NO/bradykinin pathway. Theoretical additive vasodilatory effect; no formal interaction data. Use caution if on antihypertensive therapy.
Arginine-containing peptides may affect platelet aggregation via NO signaling. No published interaction data. Monitor if combining with anticoagulation therapy; consult prescribing physician.
Pricing updated 2026-04-09
No controlled human safety data exists for Cardiogen. Not a single phase 1 trial, dose-finding study, or safety monitoring report has been published in any Western peer-reviewed journal. Every tolerability statement is extrapolated from preclinical animal work and a tiny pool of anecdotal community use. In preclinical studies, no toxicity was observed at standard experimental doses. The Khavinson group has published this across multiple papers spanning decades. But animal safety at preclinical doses does not guarantee human safety at self-administered doses, particularly when oral bioavailability is unknown and injectable protocols are community-derived rather than clinically validated. Cardiogen is composed of four common L-amino acids: alanine, glutamic acid, aspartic acid, and arginine. From a basic chemistry standpoint, acute toxicity risk is low. These amino acids are present in dietary protein. The tetrapeptide itself has an estimated half-life of 15 to 30 minutes, meaning it clears the body rapidly. Theoretical concerns are worth naming directly. Arginine is a nitric oxide precursor. Combining an arginine-containing peptide with ACE inhibitors, ARBs, or other vasodilatory medications could theoretically produce additive blood pressure effects. No formal interaction study has been conducted, so this remains speculative but worth tracking if you're on antihypertensive therapy. Arginine-containing peptides may also influence platelet aggregation through NO signaling; use caution with anticoagulants like warfarin, apixaban, or rivaroxaban. The oral capsule formulation (Cytogen brand) contains lactose as an excipient. Lactose-intolerant users may experience mild GI discomfort. This is a formulation issue, not a peptide issue. For injectable use, standard injection-site risks apply: redness, swelling, or bruising at the injection point. The reconstituted solution must be clear and colorless. Cloudiness or particulate matter means the vial should be discarded. One concern deserves direct language. Cardiogen targets cardiac tissue gene expression. The heart is not an organ where unintended gene modulation should be taken lightly. The p53 suppression mechanism, if it translates to living tissue, reduces apoptotic surveillance in cardiomyocytes. In a healthy heart, that may be irrelevant. In a heart with pre-existing pathology, the theoretical implications are less predictable. Stop immediately if you experience chest pain, palpitations, shortness of breath, or any new arrhythmia. Seek emergency medical care. Cardiogen is explicitly not a substitute for evidence-based cardiovascular treatment. Pregnant or breastfeeding individuals should avoid use entirely; no reproductive safety data exists. Children under 18 should not use this peptide. The community safety dataset is functionally nonexistent. Fewer than 20 English-language experience reports total, almost all describing multi-peptide stacks where isolating Cardiogen-specific effects is impossible.
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AEDR is a simple tetrapeptide: low synthesis cost means both high-quality and degraded products are commercially viable. No FDA oversight for research-grade supply. Russian oral Cytogen product has GMP manufacturing history but is difficult to source in the West with reliable supply chain. Injectable research vials from Western vendors have variable QC standards and no reference standard to benchmark against.
| Test | When | Target |
|---|---|---|
| Cardiac biomarkers (NT-proBNP, hs-Troponin) | Baseline before starting, especially for users with any history of cardiac disease | Normal reference ranges per laboratory standards |
| Lipid panel + CBC | Annual: for anyone running regular bioregulator protocols | — |
Not expected to change with Cardiogen use, but establishes a safety baseline. Provides evidence of no harm rather than evidence of benefit. Required context for any future cardiac evaluation.
General health monitoring. No Cardiogen-specific biomarker changes expected. Part of responsible long-term research peptide protocol management.
No noticeable effects expected. The bioregulator is proposed to begin interacting with cardiac gene expression pathways at the cellular level.
Continued gene expression modulation according to the bioregulation model. Some users anecdotally report improved exercise tolerance, though this hasn't been validated in clinical studies.
Completion of the standard treatment course. Any effects on cardiac gene expression are proposed to persist beyond the dosing period due to epigenetic mechanisms.
The bioregulatory effects are theorized to continue for several months after the course ends, with cumulative benefits from repeated courses over time.
Days 1 through 7 (Early Course): No perceptible effects are expected in the first week. If the peptide-DNA interaction mechanism is active, cardiomyocyte gene expression changes begin at the cellular level. The estimated half-life of 15 to 30 minutes means daily dosing maintains exposure, but nothing about this process produces a signal you can feel. The few community reports available describe no noticeable acute effects during this period. Mild GI discomfort from oral capsule excipients (lactose) is possible but uncommon. Days 8 through 20 (injectable) or days 8 through 30 (oral), Mid to Late Active Course: The Khavinson epigenetic model proposes cumulative effects on cardiac structural proteins (myosin heavy chain, troponin I), anti-apoptotic factors (Bcl-2, Akt), and mitochondrial biogenesis regulators (PGC-1alpha, TFAM). Anecdotal reports from LongeCity bioregulator stack threads mention improved general energy and exercise tolerance. Those effects come from multi-peptide protocols; attributing anything to Cardiogen specifically is impossible. No adverse effects have been documented in either preclinical studies or community use during this window. Months 1 through 6 (Post-Course Off-Period): Khavinson theory holds that epigenetic changes stabilize and persist for months after the course ends. Cardiomyocyte effects, if triggered, would accumulate across multiple courses over years rather than producing observable acute changes. No community reports describe withdrawal, rebound, or tolerance effects. The off-period reflects both the epigenetic persistence theory and the complete absence of long-term human safety data.
If the peptide-DNA interaction mechanism is active, cardiomyocyte gene expression modulation begins at the cellular level. Very short estimated half-life (15-30 min) means daily dosing maintains exposure. No external or perceivable signal anticipated.
No consistent community reports for this period. The few users who report experience describe no noticeable acute effects in the first week.
Continued cardiomyocyte gene expression modulation per Khavinson epigenetic model. Cumulative effects on cardiac structural proteins (myosin heavy chain, troponin I), anti-apoptotic factors (Bcl-2, Akt), and mitochondrial biogenesis regulators (PGC-1α, TFAM) are theorized to accumulate.
Anecdotal reports within Khavinson bioregulator stacks mention improved general energy and exercise tolerance: effects attributed to the overall stack, not Cardiogen specifically. No Cardiogen-isolated experience reports exist.
Khavinson theory: epigenetic changes stabilize and persist for months. Cardiomyocyte proliferative and anti-apoptotic effects, if triggered, would accumulate across multiple courses over years: not produce observable acute changes.
Insufficient independent data to characterize post-course experience. No reports of withdrawal, rebound, or tolerance effects.
Source: Estimated from general tetrapeptide degradation kinetics; no published PK data specific to cardiogen.
Loading the interactive decay curve.
Cardiogen holds no FDA approval, no EMA approval, and no regulatory clearance in any Western jurisdiction. Its regulatory status is research-only. In Russia, Cardiogen is sold commercially as an oral dietary supplement under the Cytogen brand, manufactured under Russian GMP standards. This does not constitute medical product approval by Western regulatory definitions. Western vendors sell lyophilized Cardiogen vials labeled "for research purposes only, not for human consumption." Purchasing research peptides is legal in most jurisdictions, but self-administration exists in a regulatory gray area that varies by country. Cardiogen is not listed on the 2026 WADA Prohibited List. Athletes subject to anti-doping testing should confirm current status with their governing body, as bioregulator peptides occupy an evolving regulatory space. This content is for informational purposes only and does not constitute medical advice. Cardiogen has no proven clinical efficacy in humans. Consult a qualified healthcare provider before using any research peptide.
Peptide Schedule Research TeamReviewed Apr 20265 Citations
