Cardiogen

updated

Cardiogen is the synthetic tetrapeptide Ala-Glu-Asp-Arg from the Khavinson group of Russian short-peptide bioregulators, sold for cardiac tissue repair and less local inflammation. No controlled human study exists: the record is rat heart explants, fibroblast cultures, one rat tumor study, and a heart-attack result that traces to a patent relayed by a review. Other products share the name, including a PET heart imaging agent called CARDIOGEN-82, and none of them is the peptide.

Synthetic tetrapeptide bioregulator

  • The Khavinson peptide is H-Ala-Glu-Asp-Arg-OH (AEDR): PubChem CID 11583989, C18H31N7O9, molecular weight 489.5, CAS 857267-11-9. PubChem's synonyms do not include Cardiogen, so the group's own tables tie the name to the sequence.
  • Naming warning: a PubChem name search for cardiogen returns L-carnitine, and FDA's CARDIOGEN-82 is a rubidium Rb 82 generator for PET heart imaging. Neither is the peptide.
  • In myocardial explants from 3-month-old and 24-month-old rats, the peptide at 10 to the minus 12 molar stimulated cell proliferation in both ages and lowered p53 protein expression.
  • The rat heart-attack result, a threefold decrease in mortality after coronary artery ligation, is described in a 2022 review that cites a US patent. No PubMed record of the experiment was found.
  • The one animal paper that names cardiogen is a rat sarcoma study: injections inhibited tumor growth in a dose-dependent way through hemorrhagic necrosis, acting through the tumor's vascular network.
  • A PubMed search on 10 October 2026 for cardiogen restricted to clinical trial or randomized controlled trial publication types returned 0 records.

What is Cardiogen, and is it an approved drug?

Cardiogen is the synthetic tetrapeptide Ala-Glu-Asp-Arg (AEDR) from the Khavinson group. It is not an approved drug: openFDA Drugs@FDA lists no peptide product under the name. Other products share the name, so the sequence has to stay next to it.

PubChem has a record for H-Ala-Glu-Asp-Arg-OH, CID 11583989, C18H31N7O9, molecular weight 489.5, CAS 857267-11-9, but its synonyms do not include Cardiogen. The trade name is tied to the sequence only by the group's own tables. The group's 2022 table of ultrashort peptides in the International Journal of Molecular Sciences lists Cardiogen (AEDR) as a cardioprotector and cites a US patent for it, and the group's 2021 systematic review in Molecules also lists AEDR, Cardiogen under regulation of cardiovascular system function. A 2012 abstract from the group describes the tetrapeptide H-Ala-Glu-Asp-Arg-OH and its previously reported cardioprotective activity without using the trade name.

Naming warning: other products share the name. A PubChem name search for cardiogen returns L-carnitine, not the peptide. FDA's CARDIOGEN-82 is a rubidium Rb 82 generator used as a PET heart imaging agent, a radiopharmaceutical with nothing to do with the peptide, and a ClinicalTrials.gov search for Cardiogen also returns a study of strontium exposure after CardioGen-82 scans. Nothing about either product is used as evidence on this page, and any record cited as Cardiogen needs the sequence stated to keep them apart.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry. That review sentence is the only link between the synthetic peptide and a heart extract in the records found; no study tested a heart extract or a Cytomax or Cytogen retail product.

On 10 October 2026 openFDA Drugs@FDA listed no peptide product under the name Cardiogen, and a ClinicalTrials.gov search for the peptide returned no study. This covers FDA and registry sources only and says nothing about other regulators.

PubChem: AEDR tetrapeptide identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11583989.

PubChem has a record for H-Ala-Glu-Asp-Arg-OH, CID 11583989, C18H31N7O9, molecular weight 489.5, CAS 857267-11-9, but its synonyms do not include Cardiogen, so the trade name is tied to the sequence only by the group's own tables. The group's 2022 table of ultrashort peptides in the International Journal of Molecular Sciences lists Cardiogen (AEDR) as a cardioprotector and cites a US patent for it. A 2012 abstract from the group describes the tetrapeptide H-Ala-Glu-Asp-Arg-OH and its previously reported cardioprotective activity without using the trade name, and the group's 2021 systematic review in Molecules lists AEDR, Cardiogen under regulation of cardiovascular system function.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

The record defines the sequence. The link from the name Cardiogen to the sequence rests on the group's own tables.

Read the original source
Naming warning: CARDIOGEN-82 and L-carnitine are not the peptide

Regulatory record

DailyMed, U.S. National Library of Medicine. CARDIOGEN-82 (rubidium Rb 82 generator) label record. Set ID ee95aa18-9f2f-40eb-9b4c-583bea6f36bf.

A PubChem name search for cardiogen returns L-carnitine, not the peptide. FDA's CARDIOGEN-82 is a rubidium Rb 82 generator, a PET myocardial perfusion imaging agent and a radiopharmaceutical that has nothing to do with the peptide. A ClinicalTrials.gov search for Cardiogen also returns a study of strontium exposure after CardioGen-82 scans. Any page citing a Cardiogen label, trial or PubChem record needs the sequence stated to keep these apart.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official label record for an unrelated product
Funding
not stated in the source

Naming warning only. This record is for a different product and is not evidence about the peptide.

Read the original source
2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

What did the rat and cell studies find?

In rat heart explants the peptide stimulated cell proliferation and lowered p53 protein, and in mouse embryonic fibroblasts it raised cytoskeletal protein expression 2 to 5 times. The heart-attack result comes from a patent relayed by a review, with no peer-reviewed paper found, and the one animal paper naming cardiogen is a sarcoma study.

In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. Both are explant growth and marker results, not an in vivo repair outcome.

In cultured mouse embryonic fibroblasts, H-Ala-Glu-Asp-Arg-OH raised expression of the cytoskeletal proteins actin, tubulin and vimentin by 2 to 5 times and of the nuclear matrix proteins lamin A and lamin C by 2 to 3 times. The authors conclude that the cardioprotective activity reported earlier is explained by this effect. A fibroblast culture is not heart muscle, and the abstract reports no dose.

The in vivo heart repair claim traces to a patent. The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date.

The only in vivo paper that names cardiogen is a tumor study. In senescent rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network. The abstract gives no dose or route.

2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
2012 fibroblast study: actin, tubulin, vimentin and lamins

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(4):559-62. PMID 22977870.

In cultured mouse embryonic fibroblasts, H-Ala-Glu-Asp-Arg-OH raised expression of the cytoskeletal proteins actin, tubulin and vimentin by 2 to 5 times and of the nuclear matrix proteins lamin A and lamin C by 2 to 3 times. The authors conclude that the cardioprotective activity reported earlier is explained by this effect.

Participants / model
Cultured mouse embryonic fibroblasts
Treatment
Peptide in culture medium; dose not stated in the abstract
Follow-up
not stated in the source
Study design
Cell-culture protein expression study
Funding
not stated in the source

A fibroblast culture is not heart muscle, and the abstract reports no dose. It does not use the trade name Cardiogen.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source
Rat sarcoma study: tumor growth, apoptosis, hemorrhagic necrosis

Animal study

Levdik NV et al. Bull Exp Biol Med. 2009;148(3):433-6. PMID 20396706.

In rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network.

Participants / model
Senescent rats with transplanted M-1 sarcoma
Treatment
Cardiogen injections; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical tumor model
Funding
not stated in the source

The only in vivo paper that names cardiogen. It shows the peptide acts on tumor blood vessels in this model; it is neither a safety clearance nor a finding of harm in people.

Read the original source

Has Cardiogen been tested in people?

No. A PubMed search on 10 October 2026 for cardiogen restricted to clinical trial or randomized controlled trial publication types returned 0 records, and ClinicalTrials.gov returned no study for the peptide. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data.

A PubMed search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers.

ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. Across these searches there is no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide. No human use should be implied.

PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Does Cardiogen repair heart tissue or reduce inflammation?

Cardiac tissue repair is supported only as faster growth and lower p53 in rat heart explants, plus a patent-reported drop in infarct mortality in rats that no peer-reviewed paper reproduces. Less local inflammation has no direct evidence, because no study measured an inflammatory marker after the peptide.

Sellers promote Cardiogen for cardiac tissue repair and less local inflammation. The repair claim is supported only as faster growth and lower p53 in rat heart explants, plus a patent-reported drop in infarct mortality in rats that no peer-reviewed paper found in the searches reproduces.

Less local inflammation has no direct evidence. A PubMed search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. The inflammaging language in the group's review describes hypothesized targets, not a measured result.

2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source
PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

How is Cardiogen thought to work?

The group's explanation is raised cytoskeletal and nuclear matrix protein expression, seen in mouse embryonic fibroblasts, together with lower p53 in rat heart explants. These are cell-level findings, and no pharmacokinetic data exist.

In mouse embryonic fibroblasts the peptide raised actin, tubulin and vimentin by 2 to 5 times and lamin A and lamin C by 2 to 3 times, and the authors conclude that this explains the cardioprotective activity reported earlier. In rat heart explants the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis.

The one in vivo paper that names cardiogen reports a vascular action in tumors, not a heart mechanism: in rats with transplanted M-1 sarcoma, the effect was realized through the tumor's vascular network. The heart-attack findings in the 2022 review (necrotic zones, glycogen, mitochondria) come from a patent. No human pharmacokinetics were found, and the sarcoma abstract gives no dose or route.

2012 fibroblast study: actin, tubulin, vimentin and lamins

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(4):559-62. PMID 22977870.

In cultured mouse embryonic fibroblasts, H-Ala-Glu-Asp-Arg-OH raised expression of the cytoskeletal proteins actin, tubulin and vimentin by 2 to 5 times and of the nuclear matrix proteins lamin A and lamin C by 2 to 3 times. The authors conclude that the cardioprotective activity reported earlier is explained by this effect.

Participants / model
Cultured mouse embryonic fibroblasts
Treatment
Peptide in culture medium; dose not stated in the abstract
Follow-up
not stated in the source
Study design
Cell-culture protein expression study
Funding
not stated in the source

A fibroblast culture is not heart muscle, and the abstract reports no dose. It does not use the trade name Cardiogen.

Read the original source
2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
Rat sarcoma study: tumor growth, apoptosis, hemorrhagic necrosis

Animal study

Levdik NV et al. Bull Exp Biol Med. 2009;148(3):433-6. PMID 20396706.

In rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network.

Participants / model
Senescent rats with transplanted M-1 sarcoma
Treatment
Cardiogen injections; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical tumor model
Funding
not stated in the source

The only in vivo paper that names cardiogen. It shows the peptide acts on tumor blood vessels in this model; it is neither a safety clearance nor a finding of harm in people.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source

What is known about the safety of Cardiogen?

No human safety data exist for Cardiogen. In the one animal paper that names it, the peptide inhibited sarcoma growth in rats through hemorrhagic necrosis of the tumor's vascular network, which is neither a safety clearance nor a finding of harm in people. A review's statement that these peptides have no side effects cites no safety study.

A PubMed search on 10 October 2026 found no human dose, no human pharmacokinetics and no human safety data for the peptide.

In senescent rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way through hemorrhagic necrosis, which the authors concluded was realized through the tumor's vascular network. This shows the peptide acts on tumor blood vessels in this model. It is neither a safety clearance nor a finding of harm in people.

The group's 2022 review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics. No safety study is cited for that statement.

PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source
Rat sarcoma study: tumor growth, apoptosis, hemorrhagic necrosis

Animal study

Levdik NV et al. Bull Exp Biol Med. 2009;148(3):433-6. PMID 20396706.

In rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network.

Participants / model
Senescent rats with transplanted M-1 sarcoma
Treatment
Cardiogen injections; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical tumor model
Funding
not stated in the source

The only in vivo paper that names cardiogen. It shows the peptide acts on tumor blood vessels in this model; it is neither a safety clearance nor a finding of harm in people.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source

Why does Cardiogen sit in C tier?

A defined tetrapeptide with two explant studies and fibroblast work forms a coherent but thin laboratory record, with no human data of any kind. The heart-attack result exists only as a patent relayed by a review, and the one animal paper naming cardiogen is a tumor study.

Cardiogen has a PubChem sequence record, two explant studies, fibroblast work and one animal paper that names it, a sarcoma model rather than the heart. The heart-attack mortality result exists only as a patent relayed by a review, and no peer-reviewed paper found in the searches reproduces it.

No record measures an inflammatory marker after the peptide, and a PubMed search on 10 October 2026 found no clinical trial and no human data.

PubChem: AEDR tetrapeptide identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11583989.

PubChem has a record for H-Ala-Glu-Asp-Arg-OH, CID 11583989, C18H31N7O9, molecular weight 489.5, CAS 857267-11-9, but its synonyms do not include Cardiogen, so the trade name is tied to the sequence only by the group's own tables. The group's 2022 table of ultrashort peptides in the International Journal of Molecular Sciences lists Cardiogen (AEDR) as a cardioprotector and cites a US patent for it. A 2012 abstract from the group describes the tetrapeptide H-Ala-Glu-Asp-Arg-OH and its previously reported cardioprotective activity without using the trade name, and the group's 2021 systematic review in Molecules lists AEDR, Cardiogen under regulation of cardiovascular system function.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

The record defines the sequence. The link from the name Cardiogen to the sequence rests on the group's own tables.

Read the original source
2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
Rat sarcoma study: tumor growth, apoptosis, hemorrhagic necrosis

Animal study

Levdik NV et al. Bull Exp Biol Med. 2009;148(3):433-6. PMID 20396706.

In rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network.

Participants / model
Senescent rats with transplanted M-1 sarcoma
Treatment
Cardiogen injections; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical tumor model
Funding
not stated in the source

The only in vivo paper that names cardiogen. It shows the peptide acts on tumor blood vessels in this model; it is neither a safety clearance nor a finding of harm in people.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source
PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Studies and sources

PubChem: AEDR tetrapeptide identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 11583989.

PubChem has a record for H-Ala-Glu-Asp-Arg-OH, CID 11583989, C18H31N7O9, molecular weight 489.5, CAS 857267-11-9, but its synonyms do not include Cardiogen, so the trade name is tied to the sequence only by the group's own tables. The group's 2022 table of ultrashort peptides in the International Journal of Molecular Sciences lists Cardiogen (AEDR) as a cardioprotector and cites a US patent for it. A 2012 abstract from the group describes the tetrapeptide H-Ala-Glu-Asp-Arg-OH and its previously reported cardioprotective activity without using the trade name, and the group's 2021 systematic review in Molecules lists AEDR, Cardiogen under regulation of cardiovascular system function.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined synthetic peptide
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

The record defines the sequence. The link from the name Cardiogen to the sequence rests on the group's own tables.

Read the original source
Naming warning: CARDIOGEN-82 and L-carnitine are not the peptide

Regulatory record

DailyMed, U.S. National Library of Medicine. CARDIOGEN-82 (rubidium Rb 82 generator) label record. Set ID ee95aa18-9f2f-40eb-9b4c-583bea6f36bf.

A PubChem name search for cardiogen returns L-carnitine, not the peptide. FDA's CARDIOGEN-82 is a rubidium Rb 82 generator, a PET myocardial perfusion imaging agent and a radiopharmaceutical that has nothing to do with the peptide. A ClinicalTrials.gov search for Cardiogen also returns a study of strontium exposure after CardioGen-82 scans. Any page citing a Cardiogen label, trial or PubChem record needs the sequence stated to keep these apart.

Participants / model
Not a clinical population
Treatment
Not applicable
Follow-up
Not applicable
Study design
Official label record for an unrelated product
Funding
not stated in the source

Naming warning only. This record is for a different product and is not evidence about the peptide.

Read the original source
2009 explant study: rat heart explants, proliferation and p53

Cell study

Chalisova NI et al. Adv Gerontol. 2009;22(3):409-13. PMID 20210190.

A 2009 Russian-language study describes the synthetic tetrapeptide cardiogen. In organotypic myocardial explants from 3-month-old and 24-month-old rats, the synthetic tetrapeptide at 10 to the minus 12 molar stimulated cell proliferation in both ages, and the tissue showed a decrease in p53 protein expression, which the authors read as inhibition of apoptosis. A 2006 report (PMID 17152728) found that cardiogen at 0.05 ng/ml stimulated growth in heart explants from 3-week-old and 18-month-old rats compared with control explants. A 2022 review by the same group says AEDR was detected in the polypeptide complex of the heart by chromatography with mass spectrometry; that review sentence is the only link between the synthetic peptide and a heart extract in the records found, and no study tested a heart extract or a retail Cytomax or Cytogen product.

Participants / model
Myocardial explants from young (3-month) and old (24-month) rats
Treatment
Synthetic tetrapeptide in culture medium at 10 to the minus 12 molar
Follow-up
not stated in the source
Study design
Organotypic explant culture, Russian-language study
Funding
not stated in the source

Explant growth and marker results, not an in vivo repair outcome.

Read the original source
2012 fibroblast study: actin, tubulin, vimentin and lamins

Cell study

Khavinson VKh et al. Bull Exp Biol Med. 2012;153(4):559-62. PMID 22977870.

In cultured mouse embryonic fibroblasts, H-Ala-Glu-Asp-Arg-OH raised expression of the cytoskeletal proteins actin, tubulin and vimentin by 2 to 5 times and of the nuclear matrix proteins lamin A and lamin C by 2 to 3 times. The authors conclude that the cardioprotective activity reported earlier is explained by this effect.

Participants / model
Cultured mouse embryonic fibroblasts
Treatment
Peptide in culture medium; dose not stated in the abstract
Follow-up
not stated in the source
Study design
Cell-culture protein expression study
Funding
not stated in the source

A fibroblast culture is not heart muscle, and the abstract reports no dose. It does not use the trade name Cardiogen.

Read the original source
2022 Cells review: infarct result traces to a patent

Narrative review

Khavinson V et al. Cells. 2022;12(1). PMID 36611900.

The group's 2022 review in Cells says that in rats with coronary artery ligation, AEDR gave a threefold decrease in mortality after the infarct, decreased necrotic zones, preserved glycogen in myocardial tissue, and protected mitochondria. The review cites a US patent for this, not a peer-reviewed paper, and no PubMed record of that infarct experiment was found. The same review states that these peptides cause no allergic reactions and have no side effects compared with other senolytics, an assertion with no safety study cited.

Participants / model
Rats with experimental myocardial infarction, as described in a patent and relayed by a review
Treatment
Not stated in the review text
Follow-up
not stated in the source
Study design
Review citing a patent
Funding
not stated in the source

Two 2022 reviews print different dates for the same patent number, so the patent is not cited here by number or date. The review's no-side-effects statement has no safety study behind it.

Read the original source
Rat sarcoma study: tumor growth, apoptosis, hemorrhagic necrosis

Animal study

Levdik NV et al. Bull Exp Biol Med. 2009;148(3):433-6. PMID 20396706.

In rats with transplanted M-1 sarcoma, cardiogen injections raised tumor cell apoptosis in all experimental groups and inhibited sarcoma growth in a dose-dependent way, through hemorrhagic necrosis. The authors concluded that the effect was not a direct cytostatic action and was realized through the tumor's vascular network.

Participants / model
Senescent rats with transplanted M-1 sarcoma
Treatment
Cardiogen injections; dose and route not stated in the abstract
Follow-up
not stated in the source
Study design
Preclinical tumor model
Funding
not stated in the source

The only in vivo paper that names cardiogen. It shows the peptide acts on tumor blood vessels in this model; it is neither a safety clearance nor a finding of harm in people.

Read the original source
PubMed: no clinical trial, no inflammation endpoint

PubMed search record

PubMed searches run 10 October 2026: cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]); cardiogen peptide; cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines). ClinicalTrials.gov query for cardiogen peptide AEDR and openFDA Drugs@FDA lookup, run the same day.

A PubMed search for cardiogen AND (clinical trial[pt] OR randomized controlled trial[pt]) returned 0 records. A search for cardiogen peptide returned 9 records: 4 concern the peptide (the sarcoma study, the myocardial explant study, the multi-tissue explant study and a prostate fibroblast study) and 5 are unrelated cardiac amyloid, calmodulin or cardiogenic stress papers. A search for cardiogen AND (inflammation OR inflammatory OR cytokine OR cytokines) returned 5 records, none measuring inflammation after the peptide. ClinicalTrials.gov returned no study for the query cardiogen peptide AEDR, and its 4 hits for Cardiogen alone were unrelated to the peptide. openFDA Drugs@FDA lists no peptide product under the name. The searches found no human dose, no cardiac inflammation endpoint, no human pharmacokinetics and no human safety data for the peptide.

Participants / model
Records reviewed, not a population
Treatment
Not applicable
Follow-up
Search run on 10 October 2026
Study design
Dated literature and registry search
Funding
not stated in the source

An absence finding as of 10 October 2026, not proof that no unpublished work exists.

Read the original source

Why is Cardiogen in C tier?

C fits a defined tetrapeptide with explant and fibroblast studies that add up to a coherent but thin laboratory record. There is no human data of any kind. The in vivo heart repair result comes only from a patent relayed by a review, and the one animal paper that names the peptide is a tumor study.