LongevityKEDALys-Glu-Asp-Ala

Livagen (KEDA)

Khavinson 'Cytogen' synthetic tetrapeptide · marketed as a 'liver' peptide · single-school chromatin evidence

Livagen is a synthetic tetrapeptide — four amino acids, Lys-Glu-Asp-Ala (KEDA) — from the 'Cytogen' line of short 'peptide bioregulators' developed by Vladimir Khavinson and the St. Petersburg Institute of Bioregulation and Gerontology in Russia. It is marketed within that family as the 'liver' peptide. That liver label needs an immediate caveat: it is a positioning claim, not a demonstrated effect — no primary liver study (in liver cells, liver injury, or liver protection) for Livagen could be found, so its hepatoprotective reputation is not supported by evidence. The chemistry is solid: KEDA is a well-defined molecule, and unusually for this family even the Livagen-to-sequence mapping is primary-sourced from the originating group's own paper. What the research actually shows is a specific, narrow result in cultured lymphocytes from old donors: Livagen 'decondensed' tightly packed chromatin and reactivated ribosomal genes — essentially loosening age-related DNA packaging. A separate finding is that it inhibits an enkephalin-degrading enzyme in a test-tube assay, without binding opioid receptors directly. A widely repeated claim that Livagen 'activates the interferon-gamma gene' is not found in the primary literature and is not asserted here. As with the rest of the family, every study traces to Khavinson's network and a single collaborating Tbilisi lab, with no independent external replication and no regulatory approval. The honest framing: a well-defined molecule whose only real evidence is single-school, in-vitro chromatin work on aged cells — interesting as a mechanistic showcase, but unproven as a liver or anti-aging therapy.

The short version

Livagen is a trade name for KEDA, a synthetic peptide of four amino acids (lysine, glutamic acid, aspartic acid, alanine). It comes from the Russian 'Cytogen' family of tiny 'bioregulator' peptides designed by Vladimir Khavinson's group, where each peptide is assigned a target tissue. Livagen's assigned tissue is the liver — but that is a marketing label, not a proven effect. No actual liver study (liver cells, liver injury, or liver protection) for Livagen could be found, so the hepatoprotective reputation is not backed by evidence.

The chemistry is on firm ground: KEDA is a well-defined molecule, and even the link between the name 'Livagen' and that sequence comes from the originating group's own published paper, which is more than can be said for some peptides in this family.

What the research actually demonstrates is quite specific and narrow. In cultured immune cells (lymphocytes) taken from elderly donors, Livagen loosened tightly packed DNA (chromatin) and switched certain genes back on — essentially reversing some age-related 'packing away' of genes. A separate test-tube study found it blocks an enzyme that breaks down enkephalins (natural pain-related signalling molecules), without directly hitting opioid receptors. A claim you'll often see online — that Livagen 'turns on the interferon-gamma gene' — is not found in the scientific literature and is not stated here. As with the rest of this family, all the work comes from Khavinson's network and one collaborating Tbilisi lab, with no independent replication. So Livagen is best understood as a well-defined molecule with a narrow, single-school chromatin story — not a proven liver or anti-aging treatment.

Molecular identity

Specs

Molecular formula: C₁₈H₃₁N₅O₉
Monoisotopic mass: 461.21218 Da
CAS number: Unverified — not asserted
UNII: Unverified — not asserted

Sequence (4 AA): Lys-Glu-Asp-Ala (KEDA), all-LPubChem CID 87919683; PMID 12942748 (Kost 2003)
Structure / class: Synthetic tetrapeptide; Khavinson 'Cytogen' bioregulatorPubChem CID 87919683; Khavinson-school literature
Molecular weight: 461.5 g/molPubChem CID 87919683 (displayed property value)
InChIKey: IKVDKWACACMDLR-BJDJZHNGSA-NPubChem CID 87919683
PubChem CID: 87919683 (reachable only via 'H-Lys-Glu-Asp-Ala-OH'; 'Livagen'/'KEDA' are not PubChem synonyms)PubChem
Water solubility: Highly water-soluble (computed XLogP −7.7)PubChem CID 87919683 (computed)
Molecular target: No direct opioid-receptor binding; inhibits enkephalin-degrading enzymes in vitro (IC50 ≈20 µM) and decondenses chromatin / reactivates ribosomal genes in aged-donor lymphocytes — single-schoolPMID 12942748; PMID 12533768
Half-life: Not established (no published pharmacokinetic data; only an in-vitro enzyme IC50 exists)Not established
Regulatory status: Not approved by any major drug regulator; no independent external replication locatedNo NDA/BLA/EMA record located

Plain English

Mechanism

The Khavinson school's signature thesis is that ultra-short di-, tri- and tetrapeptides penetrate cells, reach the nucleus, bind DNA in a sequence-specific way, and act as epigenetic gene-expression regulators. Livagen's chromatin-decondensation result is frequently presented as the mechanistic showcase for this whole paradigm.

It must be framed honestly: this is a single-school hypothesis with internal corroboration but minimal independent external replication, not established molecular biology. The cytogenetic readouts — scoring how condensed the chromatin looks in aged-donor lymphocytes — are also methodologically narrow and observer-dependent.

What is actually demonstrated, in the narrow sense the primary papers show, is two things. First, in cultured lymphocytes from old donors (aged 75–88), Livagen reactivated ribosomal genes and decondensed pericentromeric heterochromatin — loosening DNA that age had packed away — a result reported in the flagship 2002 paper and corroborated in a 2006 follow-up. Second, in a cell-free serum assay, Livagen inhibited enkephalin-degrading enzymes (an IC50 around 20 µM, more potent than several reference inhibitors) without binding µ- or δ-opioid receptors directly. Importantly, the widely repeated claim that Livagen 'activates the interferon-gamma gene' is not found in the primary literature and is not asserted here; the real, citable chromatin finding is ribosomal-gene reactivation, not interferon-gamma activation.

Sources:PMID 12533768 PMID 12942748 PMID 16705247

Why people reach for it

Potential benefits

Livagen (KEDA) is sold as the Khavinson family's 'liver' peptide, but its actual evidence is a narrow chromatin story in aged cells. Here's what draws people to it — kept honest about how little sits underneath, especially the liver label.

An epigenetic / cellular-aging showcase — Livagen's one real result is striking on paper: in lymphocytes from elderly donors it loosened age-condensed DNA and switched ribosomal genes back on — the chromatin-reactivation finding people reach for it on, though it's in-vitro and single-school, not a human outcome.
A liver-support angle people pursue — It's marketed and used as a liver peptide, which is the reason most people try it — but worth flagging plainly: no primary liver study (liver cells, injury, or protection) for Livagen exists, so the hepatic reputation is positioning, not a demonstrated effect.
Used within longevity / anti-aging protocols — Because its chromatin finding is framed as reversing age-related gene 'packing away', it's reached for in broad healthy-aging routines — an aspiration drawn from a mechanistic showcase, not proven rejuvenation.
Runs as a short, defined course — Like the rest of the family, Livagen is used in brief pulsed courses (often 10–14 days) rather than daily indefinitely — a contained pattern that suits the bioregulator approach.
Pairs more sensibly with the actual liver antioxidant — Rather than only stacking other single-school bioregulators, the more defensible pairing is with Glutathione — the liver's real master antioxidant — which contributes measurably where Livagen's liver claim is unproven.

Sources:PMID 12533768 PMID 16705247 PMID 12942748

What people reach for Livagen for, drawn from what the research reports (single-school, in-vitro chromatin work) and how it's used — not proven human outcomes or medical claims. The 'liver' identity is positioning, not demonstrated.

Implied timing

Best time to dose

Implied best time

Anytime (consistent)

Time of day isn't critical for Livagen — pick one daily time you'll actually keep, and hold it across the course.

Livagen is positioned as a liver/organ-support bioregulator, not a circadian one. Nothing in its proposed mechanism (chromatin reactivation in cells, enkephalin-enzyme inhibition in a test tube) ties its effect to a particular time of day.
Unlike the pineal members of this family (Epitalon, Pinealon), there's no melatonin or body-clock logic pulling Livagen toward the evening, and no daytime-cognition reason pulling it toward the morning — so any consistent slot is reasonable.
No published human pharmacokinetic or chronobiology data exist for Livagen, so consistency is the only defensible timing guidance; morning is a common default simply because it's easy to remember, not because it's better.
Livagen is run in short pulsed courses (often 10–14 days), so holding the same daily time across the course is what actually matters.

No study establishes an ideal time of day for Livagen — this is reasoned from its organ-support (non-circadian) mechanism and how it's used. As a rule of thumb most peptide dosing lands in the midday-to-evening window; for Livagen the time of day isn't critical, so consistency is the verdict.

How to run it

Dosing & protocol

Livagen is dosed here as a subcutaneous injection — the form sold as a research peptide and the route the on-page calculator is built for. There is no published human dose of any kind: the entire evidence base is in-vitro (cell and serum assays). The ranges below are community convention only, extrapolated from how the Khavinson school positions KEDA as a short 'bioregulator' tetrapeptide. Read this as a map of how people actually run injectable Livagen — not a validated prescription.

Community convention, not trial-proven: Livagen has no human trial and no published human dose. Its only quantitative figure is an in-vitro enzyme IC50 (~20 µM), not a dose. Every number here is a usage pattern, not evidence.

Dose — no established human dose

No controlled human or animal in-vivo dose exists for Livagen. The convention below is based entirely on how the Khavinson-school 'bioregulator' tetrapeptides are collectively used, not on any trial finding.

Convention range:: 100–500 mcg per injection subcutaneously — the range most often cited in Khavinson-influenced community protocols for the short bioregulator tetrapeptides. No dose-response data exist to support any tier within this range over another.
Frequency:: Once daily in a morning injection is the most common community convention for pulsed bioregulator courses. Some protocols cite once-daily for 10-day blocks; the biological rationale is entirely the school's 'brief peptide pulse per tissue' framework, not a trial.
Route:: Subcutaneous injection (SubQ) — into the fat layer of the abdomen or outer thigh. This is the route the calculator is built for and the standard for research-peptide vials. No pharmacokinetic comparison of routes exists for Livagen.

Subcutaneous administration

Livagen is injected into subcutaneous fat; site rotation and timing are the actionable choices.

Injection site:: The abdomen (staying a couple of inches clear of the navel) or the outer thigh. Rotate sites between doses — using the same spot repeatedly causes local irritation and fatty lumps (lipohypertrophy).
Measuring the dose:: Drawn on a U-100 insulin syringe from the reconstituted vial. At the standard calculator defaults (10 mg vial + 2 mL bacteriostatic water = 5,000 mcg/mL): 100 mcg = 2 IU · 200 mcg = 4 IU · 500 mcg = 10 IU. The on-page calculator handles any vial size.
Time of day:: Time of day isn't critical for Livagen — see Best time to dose above. Morning is a common default (in line with the school's 'activating pulse' positioning), but no circadian or pharmacokinetic data exist for Livagen specifically, so holding a consistent daily time across the course matters more than the exact hour.
Food window:: SubQ peptides bypass digestion, so Livagen can be injected without regard to meals.

Cycle & washout

Khavinson-school bioregulators are conventionally run as short pulsed courses rather than continuous use — the rationale is to deliver a brief gene-regulatory signal, not sustained receptor occupation.

Course length:: 10-day courses are the most widely cited convention in the school's own clinical write-ups (though those are not controlled trials). Some community users run 2–4-week cycles. No data distinguish one duration from another.
Washout:: The school typically describes a washout of several months between courses — the logic being that the peptide 'reactivates' dormant genes and then the body's own expression carries forward. In practice, community cycles range from 4–12 weeks on, 4–8 weeks off.
Re-assessment:: With no validated biomarker for Livagen's proposed chromatin effect in humans, there is no objective measure to reassess between cycles. General liver-function panels (ALT/AST/GGT) might track the organ whose health motivates many users — though they would reflect liver health generally, not a Livagen effect specifically.

Reconstitution at a glance

The on-page calculator does this live. Quick reference for a 10 mg vial at the calculator's default (2 mL bacteriostatic water):

Mixing:: 10 mg vial + 2 mL bacteriostatic water = 5,000 mcg per mL. On a U-100 (1 mL) insulin syringe: 100 mcg = 2 IU · 200 mcg = 4 IU · 250 mcg = 5 IU · 500 mcg = 10 IU.
Note on concentration:: The 2 mL default gives a relatively concentrated solution — suitable when convention doses are in the lower end of the range (100–200 mcg). For larger volumes that make small doses easier to measure precisely, use the calculator to adjust.

Sources:PMID 12533768 PMID 12942748

Substrate the signal needs

Nutritional cofactor precision

Livagen is marketed as a liver peptide — but that is positioning, not a demonstrated effect. The useful cofactors here are the nutrients the liver's own metabolism and antioxidant defence actually run on: supply the substrate, and support the organ's proven biochemical levers independently of whether Livagen does anything.

Reasoned from liver biochemistry and the proposed liver-support target — not a Livagen cofactor study. None of these 'treat' the liver; they supply the substrate the liver's own chemistry depends on. Supplement doses are standard community ranges.

Supply the substrate — choline, NAC + glutathione, methylation B-vitamins

The liver's three core biochemical demands: fat-export capacity (choline), master antioxidant defence (glutathione via NAC), and methylation throughput (B-vitamins).

Choline — 400–550 mg/day:: The liver uses choline to assemble the phospholipid shell around fat particles (VLDL) and export them into circulation. Low choline is a well-established driver of fat accumulation in liver cells (hepatic steatosis). Eggs, liver, and lecithin are food sources; CDP-choline or alpha-GPC at 400–550 mg are the supplement forms. Timing: with meals.
NAC (N-acetylcysteine) — 600 mg/day:: NAC is the direct precursor to cysteine, the rate-limiting amino acid for glutathione synthesis. The liver uses glutathione as its primary antioxidant — it neutralises reactive oxygen species and is central to phase-II detoxification. 600 mg once daily is the standard range; taken with food to reduce the mild nausea some users report.
Methylation B-vitamins (folate, B12, B6, riboflavin):: Methylation is a core liver reaction — used for fat processing, homocysteine clearance, and phase-II conjugation. A B-complex supplying 400 mcg methylfolate + 500–1,000 mcg methylcobalamin (B12) + 25–50 mg B6 + 10–25 mg riboflavin covers the full set. Taken in the morning with food.

Amplify — milk thistle and the proven lifestyle levers

Silymarin (milk thistle) is the best-evidenced botanical for liver support. The truly proven levers are lifestyle, not supplements — named here honestly.

Silymarin (milk thistle extract) — 140–420 mg/day:: Silymarin is the active flavonolignan complex in milk thistle. It has the strongest human evidence of any botanical in the liver-support category — multiple RCTs in alcoholic liver disease and non-alcoholic fatty liver show modest improvements in transaminases (ALT/AST). 140–420 mg standardised to 70–80% silymarins, taken with food. This is the best-evidenced lever in this stack; it works independently of Livagen and does not depend on Livagen's unproven liver identity.
Alcohol moderation and not overfeeding (NAFLD prevention):: The most potent documented liver-health interventions are behavioural: eliminating excess alcohol and avoiding chronic caloric surplus are the two primary causes of fatty liver disease. No supplement or peptide overrides these inputs. Honest framing: if the goal is liver health, these two changes deliver more measurable benefit than any molecule on this page.

Mitigate — minimal

Livagen's evidence base is in-vitro and does not establish a side-effect profile, so there is no identified cost to mitigate.

Selenium — 100–200 mcg/day:: Selenium is a cofactor for glutathione peroxidase and thioredoxin reductase — the enzymes that recycle glutathione after it has neutralised an oxidant. If NAC is being used to boost glutathione, adequate selenium ensures the recycling enzymes can keep pace. Brazil nuts (1–2 per day) or a selenomethionine supplement at 100–200 mcg. Do not exceed 400 mcg/day (toxicity threshold).

Combinations + timing

Stacking notes + timing windows

Livagen is most often discussed as part of the wider Khavinson bioregulator family — 'a different peptide per tissue' — rather than as a standalone. The honest caveat leads: stacking multiple single-school bioregulators multiplies the speculation proportionally, since each individual peptide is thinly evidenced and none have been studied together. The more defensible companion here is Glutathione itself — the actual liver antioxidant that the cofactor section is trying to supply via NAC.

Combinations reasoned from the Khavinson school's tissue-specific framework and liver biochemistry — not studied head-to-head. Livagen itself has no human trial; any stack is doubly unproven. Doses are community convention. 'Reached for' describes where users go, not a proven indication.

Livagen + Epitalon

The most common Khavinson pairing — 'liver' + 'pineal', the two most discussed members of the bioregulator family.

Why it works (claimed):: Within the Khavinson framework, Epitalon is positioned as the pineal/telomere peptide and Livagen as the liver peptide — two different tissue targets, so the school's logic treats them as non-overlapping. The 2006 Lezhava study showed both produce similar chromatin-reactivation patterns in aged lymphocytes, which is the school's shared mechanistic rationale.
The protocol:: Livagen 100–500 mcg SubQ once daily + Epitalon 5–10 mg SubQ once daily (Epitalon's community convention), both as pulsed 10–14-day courses. Honesty note: stacking two single-school, in-vitro-only, unvalidated peptides is doubly speculative. The school's 'different tissue' logic has not been tested in any controlled setting.
Outcome:: Used by people following the full Khavinson bioregulator protocol as part of a tissue-coverage routine — not for any synergy demonstrated in a study.

Livagen + Glutathione (injectable)

A more defensible pairing: if the goal is liver antioxidant support, the actual liver antioxidant — Glutathione — is a more established companion than any other bioregulator peptide.

Why it works:: Glutathione is the liver's master antioxidant — directly measured, depleted in liver stress, and replenished by intravenous or SubQ administration. Pairing it with Livagen does not depend on Livagen's unproven liver claim to be useful: glutathione contributes measurably while Livagen contributes speculatively. Different mechanisms — the pairing doesn't stack the same lever twice.
The protocol:: Livagen 100–500 mcg SubQ once daily + glutathione 200–600 mg SubQ (reduced L-glutathione, the injectable form) once daily or on alternating days. The NAC cofactor card above is an oral alternative to injectable glutathione for those who prefer to work upstream.
Outcome:: Reached for as a liver-antioxidant support combination — with the honest acknowledgement that glutathione's contribution is grounded in biochemistry, while Livagen's is unproven positioning.

Livagen + Vilon

The Khavinson family's immune-member addition — 'liver' + 'thymus/immune' within the school's tissue-specific framework.

Why it works (claimed):: Vilon (Lys-Glu) is the Khavinson school's thymic bioregulator; Lezhava 2006 showed Vilon and Livagen both produce chromatin-reactivation in aged lymphocytes. The school pairs them on a 'different tissue targets' basis. No head-to-head study of the combination exists.
The protocol:: Livagen 100–500 mcg SubQ once daily + Vilon 100–500 mcg SubQ once daily, as concurrent or sequential 10-day pulsed courses. Honesty note: multiplying single-school, in-vitro-only peptides linearly multiplies the speculation. The liver claim for Livagen is unproven; the immune claim for Vilon is similarly thin.
Outcome:: Used within the full Khavinson multi-peptide protocol as a liver + immune tissue-coverage pairing — not a synergy demonstrated in a controlled study.

Reconstitution math

Reconstitution calculator

Calculated for a 1 mL U-100 insulin syringe (100 units/mL).

Peptide per vial

BAC water added

Desired dose

Units per dose

Draw to this mark on a U-100 syringe

Volume per dose: 0.2 mL
Doses per vial: 10
Concentration: 5 mg/mL

One vial lasts

Daily: 10 days
Every other day: 20 days
5×/week: 14 days

Research use only. Not for human consumption. Outputs are reference values based on research literature — verify all measurements independently.

From the studies

Side effects from research

There is no meaningful human safety database for Livagen. The research is entirely in-vitro cell and serum work, which cannot characterise side effects, rare events, or long-term risk in people. There are no controlled human or even animal in-vivo safety studies to draw on.

Because there is effectively zero controlled human exposure, nothing can be said with confidence about safety at any dose, over any duration. The marketed 'liver' framing is particularly worth flagging here, since it might imply a reassuring organ-supporting profile that the evidence simply does not establish.

Gray-market sourcing adds purity and identity risk independent of the peptide. The honest summary: Livagen's human safety is uncharacterised, not established.

Sources:PMID 12533768

As reported in literature

Research dosing ranges

These are in-vitro experimental settings — all from the Khavinson network and its Tbilisi collaborators — shown for reference only. There is no human or animal dose, no approved regimen, and no independent replication. The one quantitative figure (an enzyme IC50 around 20 µM) is a test-tube potency value, not a dose.

Dose	Route	Model	Outcome	Sources:
In vitro	Cell culture	Cultured lymphocytes from old donors (75–88 yr) (Khavinson 2002, Bull Exp Biol Med — the flagship chromatin paper)	Livagen reactivated ribosomal genes, decondensed pericentromeric heterochromatin, and released age-repressed genes — a chromatin-loosening signal in aged cells, not a clinical outcome (note: this is ribosomal-gene reactivation, NOT interferon-gamma activation)	PMID 12533768
IC50 ≈ 20 µM	Cell-free assay	Human serum enkephalin-degrading enzyme assay (Kost 2003, Izv Akad Nauk Ser Biol)	Livagen (defined as Lys-Glu-Asp-Ala) inhibited enkephalinase, IC50 ≈ 20 µM, more potent than puromycin/leupeptin; no direct µ/δ-opioid receptor binding — a biochemical potency value, not a dose	PMID 12942748
In vitro	Cell culture	Old-donor lymphocytes; Epitalon, Livagen, Vilon (Lezhava 2006, Georgian Med News)	All three reactivated chromatin (ribosomal-gene/NOR reactivation, heterochromatin decondensation) in old-donor lymphocytes — corroborates the chromatin finding within the same network	PMID 16705247
In vitro	Cell culture	Lymphocyte chromatin in senile subjects (Khavinson 2004, Bull Exp Biol Med)	Short peptides including Livagen affected lymphocyte chromatin in senile subjects — a further single-school chromatin observation	PMID 15085253

Quick answers

Frequently asked

What is Livagen?

It is a trade name for KEDA, a synthetic tetrapeptide (Lys-Glu-Asp-Ala) from Vladimir Khavinson's Russian 'Cytogen' line of short peptide bioregulators, marketed as the 'liver' peptide. The molecule is well-defined chemically; the liver and anti-aging claims are single-school and, in the case of liver effects, not supported by any primary study.

Is Livagen actually good for the liver?

There is no evidence for that. No primary liver study (liver cells, liver injury, or liver protection) for Livagen could be found — the 'liver peptide' label is marketing positioning, not a demonstrated effect. The only real evidence is in-vitro chromatin work in immune cells from elderly donors.

Does Livagen activate the interferon-gamma gene?

That claim is widely repeated online but is not found in the primary scientific literature, so it is not asserted here. The actual, citable chromatin finding is reactivation of ribosomal genes and loosening of age-condensed DNA in aged-donor lymphocytes — not interferon-gamma activation.

How does it supposedly work?

The Khavinson school proposes that this small peptide enters the nucleus and binds DNA to regulate genes; Livagen's chromatin-loosening result is often used as the showcase for that idea. But it is a single-school hypothesis with little independent replication. What is actually shown is reactivation of ribosomal genes and heterochromatin decondensation in cultured aged cells, plus enzyme inhibition in a test tube.

Is there a known dose, and is it approved?

There is no citable dose — the research is in vitro, and the only number (an enzyme IC50 around 20 µM) is a potency value, not a dose. Livagen is not approved by any major drug regulator, and no independent group outside the Khavinson network has replicated its findings.

Primary sources

References

PMID 12533768Khavinson VKh, Lezhava TA, Monaselidze JG et al., Bull Exp Biol Med 2002 — flagship: Livagen reactivates ribosomal genes and decondenses pericentromeric heterochromatin in old-donor lymphocytes
PMID 12942748Kost NV et al., Izv Akad Nauk Ser Biol 2003 — Livagen (defined as Lys-Glu-Asp-Ala) inhibits serum enkephalin-degrading enzymes, IC50 ≈20 µM; no µ/δ-opioid receptor binding (primary-sources the KEDA sequence)
PMID 16705247Lezhava T, Monaselidze J, Kadotani T et al., Georgian Med News 2006 — Epitalon, Livagen, Vilon reactivate chromatin (ribosomal-gene/NOR reactivation, heterochromatin decondensation) in old-donor lymphocytes
PMID 15085253Khavinson VKh, Lezhava TA, Malinin VV, Bull Exp Biol Med 2004 — short peptides (incl. Livagen) affect lymphocyte chromatin in senile subjects
PMID 17460203Lezhava T, Jokhadze T, Ann N Y Acad Sci 2007 — peptide-induced activation of pericentromeric/telomeric heterochromatin in old-individual lymphocytes
PubChem CID 87919683PubChem record — identity (CID, formula, MW, sequence). Reachable only via 'H-Lys-Glu-Asp-Ala-OH'; 'Livagen'/'KEDA' are not PubChem synonyms

Research use only · Not medical advice · Updated 2026-06-01