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Best Peptides for Liver Health & Repair

Your liver handles over 500 functions every day. It filters toxins, metabolizes drugs, produces bile, stores energy, and synthesizes proteins your blood needs to clot.

Your liver handles over 500 functions every day. It filters toxins, metabolizes drugs, produces bile, stores energy, and synthesizes proteins your blood needs to clot. When it gets damaged — by alcohol, medications, viral infections, metabolic disease, or even radiation — the consequences ripple through your entire body.

The problem: liver disease is often silent until it's advanced. By the time symptoms appear, significant damage may already be in place. That's why researchers have been studying hepatoprotective peptides — short chains of amino acids that may protect liver cells, reduce fibrosis, and support regeneration.

This guide covers the most promising peptides for liver health based on current research, from well-studied compounds like BPC-157 to FDA-approved GLP-1 receptor agonists now being used for fatty liver disease.

Table of Contents

How the Liver Gets Damaged — and How It Heals

Before looking at specific peptides, it helps to understand what goes wrong in liver disease and what "repair" actually means at the cellular level.

Liver damage typically follows a predictable sequence:

  1. Initial insult — Toxins, viruses, fat accumulation, or ischemia injure hepatocytes (liver cells)
  2. Inflammation — Immune cells flood the area, releasing pro-inflammatory cytokines like TNF-alpha and IL-6
  3. Oxidative stress — Reactive oxygen species (ROS) overwhelm the liver's antioxidant defenses
  4. Stellate cell activation — Normally quiet hepatic stellate cells "wake up" and start producing collagen
  5. Fibrosis — Excess collagen and extracellular matrix proteins replace healthy liver tissue with scar tissue
  6. Cirrhosis — If fibrosis continues unchecked, the liver becomes permanently scarred and loses function

The good news: the liver has remarkable regenerative capacity. Unlike most organs, it can regrow functional tissue if the underlying damage is controlled. Hepatoprotective peptides target multiple stages of this damage cascade — reducing inflammation, neutralizing oxidative stress, blocking fibrosis pathways, and supporting hepatocyte survival.

BPC-157: The Most Studied Hepatoprotective Peptide

BPC-157 (Body Protection Compound-157) is a 15-amino acid peptide derived from a protein found in human gastric juice. It's been studied for liver protection since the early 1990s, making it one of the most well-documented hepatoprotective peptides in preclinical research.

What the Research Shows

The foundational study on BPC-157 and liver health was published in Life Sciences in 1993. Researchers tested BPC-157 in three different models of liver injury in rats: bile duct ligation combined with hepatic artery ligation, restraint stress, and carbon tetrachloride (CCl4) poisoning [1].

The results were consistent across all three models. BPC-157, given either orally or by injection, significantly prevented liver necrosis and fatty changes. The comparison drugs — bromocriptine, amantadine, and somatostatin — showed little to no protective effect in the same models. Laboratory markers including bilirubin, SGOT, and SGPT correlated with the visible tissue improvements.

More recent work has expanded these findings:

Radiation-induced liver disease (2022): A study published in Life Sciences found that oral BPC-157 reduced radiation-induced liver injury in mice exposed to 12 Gy radiation. The peptide lowered AST and ALT levels, decreased hepatic lipid accumulation, and reduced liver cell death. The protective effect worked through upregulation of Kruppel-like factor 4 (KLF4) — when researchers knocked down KLF4, BPC-157's protective effects disappeared [2].

Ischemia-reperfusion injury (2025): A study published in Medicina evaluated BPC-157's effects on distant organ damage following lower-extremity ischemia-reperfusion injury in rats. BPC-157 reduced oxidative stress markers and histopathological damage in liver, kidney, and lung tissue simultaneously. Total antioxidant status improved significantly in the BPC-157-treated group [3].

Inflammatory cytokine suppression: In bile duct-ligated rats, BPC-157 therapy reduced NOS3 expression and lowered IL-6, TNF-alpha, and IL-1-beta levels in liver tissue — three key inflammatory drivers of liver damage [4].

How BPC-157 Protects the Liver

The mechanisms appear to work on multiple fronts:

  • Anti-inflammatory: Reduces pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1-beta)
  • Antioxidant: Neutralizes free radicals and increases antioxidant enzyme expression
  • Anti-fibrotic: Downregulates factors that promote collagen deposition and scarring
  • Cytoprotective: Protects hepatocytes from apoptosis (programmed cell death)
  • Vascular: Supports angiogenesis and blood vessel repair in damaged liver tissue

For a deeper look at the full range of BPC-157 research, see our BPC-157 complete guide.

GLP-1 Receptor Agonists: Semaglutide and Tirzepatide for Fatty Liver

GLP-1 receptor agonists represent the most clinically advanced peptide therapy for liver disease. Unlike most peptides on this list, semaglutide and tirzepatide are FDA-approved medications with human clinical trial data.

The NAFLD/NASH Connection

Non-alcoholic fatty liver disease (NAFLD) — now called metabolic dysfunction-associated steatotic liver disease (MASLD) — affects roughly 25% of adults worldwide. About 20% of those progress to non-alcoholic steatohepatitis (NASH), where fat accumulation leads to inflammation and liver damage. NASH can progress to fibrosis, cirrhosis, and liver cancer.

GLP-1 receptor agonists were originally developed for type 2 diabetes and obesity, but researchers noticed they also improved liver markers. That observation triggered dedicated clinical trials.

Key Clinical Trial Results

Phase 2 NASH trial (NEJM, 2021): In a 72-week, double-blind trial of patients with biopsy-confirmed NASH and fibrosis stages F1-F3, daily subcutaneous semaglutide at 0.4 mg achieved NASH resolution without worsening of fibrosis in 59% of patients — compared to 17% on placebo. That's an odds ratio of 6.87, the highest response rate any drug has achieved in a NASH trial to date [5].

Real-world evidence (2022): A 52-week prospective study in patients with type 2 diabetes found that once-weekly semaglutide progressively reduced liver enzyme concentrations and improved hepatic steatosis scores. Eighty percent of responders showed at least a one-class improvement in liver steatosis severity [6].

Tirzepatide: As a dual GIP/GLP-1 receptor agonist, tirzepatide may offer even greater metabolic benefits for liver health. Clinical trials are ongoing, and next-generation triple agonists (GLP-1/GIP/glucagon) like retatrutide and survodutide are also being studied for NASH.

How GLP-1 Agonists Help the Liver

  • Weight loss reduces hepatic fat content directly
  • Improved insulin sensitivity decreases hepatic lipogenesis (fat production in the liver)
  • Anti-inflammatory effects reduce liver inflammation independent of weight loss
  • Reduced lipotoxicity protects hepatocytes from fat-induced damage

The Fibrosis Question

One consistent limitation: GLP-1 agonists have not yet demonstrated significant improvement in liver fibrosis in clinical trials. A phase 2 study of semaglutide 2.4 mg in patients with NASH-related cirrhosis found improvements in metabolic markers and liver fat but no significant fibrosis regression [7]. A phase 3 trial (NCT04822181) scheduled to run for 5 years is evaluating semaglutide's long-term effects on liver-related clinical events.

Thymosin Beta-4 (TB-500): Anti-Fibrotic Liver Protection

TB-500 is a synthetic fragment of thymosin beta-4, a 43-amino acid peptide found in nearly all mammalian cells. It's best known for tissue repair research, but a growing body of preclinical evidence points to specific liver-protective effects.

Alcohol-Induced Liver Injury

A 2018 study in mice found that thymosin beta-4 reduced inflammation, oxidative stress, and fibrosis in alcohol-induced liver injury. The peptide appeared to prevent the activation of hepatic stellate cells — the key drivers of liver scarring [8].

Carbon Tetrachloride Liver Damage

Researchers also tested exogenous thymosin beta-4 against CCl4-induced acute liver injury and fibrosis. The peptide prevented acute damage and subsequent fibrotic changes by reducing oxidative stress and inflammation [9].

Preventing Hepatocyte Death

One of the more interesting findings involves thymosin beta-4's ability to block hepatocyte apoptosis. Research showed that Tβ4 reversed the expression of pro-apoptotic factors (cleaved caspase-3 and caspase-9) that drive liver cell death, a process that leads to fibrosis and cirrhosis if it continues unchecked [10].

Hepatic Stellate Cells

A 2015 study published in PLoS ONE examined how hepatic stellate cells — the cells responsible for producing scar tissue — express thymosin beta-4 in chronically damaged liver tissue. This suggests that TB-500 may work partly by modulating these cells' behavior during liver injury [11].

Safety Data

Phase I clinical trials of injectable recombinant human thymosin beta-4 in healthy adults showed no toxicities or serious adverse events. Liver function tests remained normal throughout. However, long-term safety data beyond several months remain limited.

For more on TB-500's tissue repair mechanisms, see our TB-500 research guide.

GHK-Cu: The Liver Cell Growth Factor

Here's a fact that surprises most people: GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) was originally discovered as a liver cell growth factor. The peptide we now know primarily for skin and hair benefits has deep roots in hepatology.

The Discovery

In 1973, researcher Loren Pickart noticed something unusual. Liver tissue from patients aged 60-80 had elevated fibrinogen and reduced function. But when those older liver cells were incubated in blood serum from younger donors, they started functioning more like young liver cells. The active factor turned out to be GHK — a small tripeptide with a high affinity for copper [12].

GHK was subsequently described as a hepatotrophic agent — a substance that promotes liver cell growth and stimulates hepatic erythropoietic factor production.

Anti-Fibrotic Properties

GHK-Cu's relevance to liver disease goes beyond cell growth. The peptide has demonstrated anti-fibrotic effects across multiple organ models:

  • Downregulates TGF-beta-1, a key driver of fibrosis in the liver and other organs [13]
  • Suppresses TNF-alpha and IL-6, reducing the inflammatory signals that trigger stellate cell activation
  • At concentrations as low as 10 micromolar, GHK reduces reactive oxygen species (ROS) levels by nearly 50% in cell models — stronger hydroxyl radical quenching than glutathione [14]

GHK naturally declines with age. Serum levels average 200 ng/mL at age 20 and drop to 80 ng/mL by age 60 [15]. This decline may partially explain age-related increases in liver fibrosis susceptibility.

Gene Expression

Broad gene expression studies show GHK-Cu influences over 4,000 human genes, many related to tissue repair, inflammation, and extracellular matrix remodeling. This wide-ranging gene modulation may explain why its effects appear across so many organ systems.

For the full picture on GHK-Cu research, see our GHK-Cu science guide.

KPV: Gut-Liver Axis and Inflammation Control

KPV (Lys-Pro-Val) is a tripeptide fragment of alpha-melanocyte-stimulating hormone (alpha-MSH). Its connection to liver health is indirect but physiologically important — it works through the gut-liver axis.

The Gut-Liver Axis Connection

Your gut and liver are connected by the portal vein, which carries blood directly from the intestines to the liver. When the gut barrier breaks down — a condition called intestinal permeability or "leaky gut" — bacterial products, inflammatory molecules, and toxins flow straight to the liver. This is a recognized driver of liver inflammation and NAFLD progression.

KPV's primary action is reducing intestinal inflammation. In mouse models of colitis, orally delivered KPV decreased disease severity, reduced pro-inflammatory cytokines (TNF-alpha and IL-6), and preserved gut barrier function [16]. The peptide enters intestinal epithelial cells via the PepT1 transporter and directly inhibits inflammatory signaling pathways inside the cell, including NF-kB.

Why This Matters for the Liver

By reducing gut inflammation and maintaining barrier integrity, KPV may limit the flow of pro-inflammatory signals reaching the liver through the portal circulation. While direct studies of KPV on liver tissue are limited, the gut-liver connection is well established in hepatology research. Intestinal dysbiosis and increased intestinal permeability are consistently associated with the progression of liver diseases ranging from NAFLD to alcoholic hepatitis.

For more on KPV's anti-inflammatory properties, see our KPV profile. You can also explore how gut health peptides work together in our best peptides for gut health guide.

Humanin: Mitochondrial Protection for Hepatocytes

Humanin is a 24-amino acid peptide encoded by mitochondrial DNA — not nuclear DNA. First discovered in 2001 for its neuroprotective properties, it has since been studied for metabolic effects across multiple organs, including the liver.

Liver-Specific Effects

Humanin appears to directly influence hepatic metabolism:

  • Lipid metabolism: Treatment of human hepatocytes with humanin decreased lipid accumulation and downregulated lipogenesis genes including SREBP1, FAS, and SCD1. This is directly relevant to NAFLD, where hepatic fat accumulation is the initiating event [17].
  • Insulin sensitivity: Humanin increases insulin-mediated AKT signaling in the liver, enhancing glucose uptake peripherally while inhibiting hepatic glucose production [18].
  • Anti-apoptotic effects: Humanin protects against oxidative stress-induced cell death across multiple organ systems, including the liver.

The Aging Connection

Like GHK-Cu, humanin levels decline with age. This natural decline may contribute to the increased susceptibility to metabolic liver disease seen in older adults. Patients with chronic kidney disease show elevated circulating humanin — interpreted as a stress response attempting to protect against ongoing metabolic damage.

For more on mitochondrial-derived peptides, see our guides on humanin and MOTS-c.

Peptide Comparison Table

PeptidePrimary Liver MechanismResearch StageKey EvidenceRoute
BPC-157Anti-inflammatory, antioxidant, cytoprotectivePreclinical (animal studies)Protected against CCl4, radiation, and ischemia-reperfusion liver injuryOral, injection
SemaglutideFat reduction, insulin sensitization, anti-inflammatoryPhase 2/3 clinical trials (human data)59% NASH resolution rate vs. 17% placebo (NEJM 2021)Injection, oral
TirzepatideDual GIP/GLP-1 agonism, weight loss, metabolic improvementClinical trials ongoingStrong metabolic improvements; liver-specific trials underwayInjection
TB-500Anti-fibrotic, anti-apoptotic, stellate cell modulationPreclinical (animal studies)Reduced alcohol-induced and CCl4-induced liver injury in miceInjection
GHK-CuLiver cell growth factor, TGF-beta suppression, antioxidantPreclinical (in vitro + animal)Originally discovered as hepatotrophic agent; anti-fibrotic in organ modelsTopical, injection
KPVGut-liver axis protection, NF-kB inhibitionPreclinical (animal studies)Reduced intestinal inflammation in colitis modelsOral
HumaninHepatic lipid metabolism, anti-apoptoticPreclinical (in vitro + animal)Decreased hepatocyte lipid accumulation; improved insulin signalingInjection

Important Caveats About Peptide Research

A few things to keep in mind as you evaluate this research:

Most evidence is preclinical. With the exception of GLP-1 receptor agonists (semaglutide, tirzepatide), the peptides covered here have been studied primarily in cell cultures and animal models. Rodent results don't always translate to humans.

GLP-1 agonists are the only FDA-approved option. Semaglutide and tirzepatide have undergone rigorous human trials and are prescribed by physicians. The other peptides on this list are not FDA-approved for liver disease treatment.

Peptides are not substitutes for medical treatment. If you have diagnosed liver disease — NAFLD, NASH, hepatitis, cirrhosis — work with a hepatologist or gastroenterologist. Peptides may eventually complement standard therapies, but they don't replace them.

Quality matters. For non-FDA-approved peptides, product quality varies dramatically. Contaminants, incorrect sequences, and impurities in low-quality products can themselves cause liver and kidney damage. If a peptide is contaminated with heavy metals or endotoxins, it may harm the very organ you're trying to protect.

Lifestyle remains foundational. No peptide compensates for excessive alcohol consumption, poor diet, or uncontrolled metabolic disease. Weight loss alone (through any means) reduces liver fat and inflammation.

Frequently Asked Questions

Can peptides reverse liver damage?

That depends on the type and extent of damage. The liver has strong regenerative capacity, and preclinical studies show several peptides (BPC-157, TB-500, GHK-Cu) can reduce fibrosis markers and support hepatocyte survival in animal models. GLP-1 agonists like semaglutide have demonstrated NASH resolution in human trials. However, advanced cirrhosis with established scarring is much harder to reverse than early-stage fibrosis or steatosis.

Are hepatoprotective peptides safe for people with existing liver disease?

GLP-1 receptor agonists have been tested in patients with liver disease, including NASH-related cirrhosis, and showed acceptable safety profiles. For other peptides (BPC-157, TB-500, GHK-Cu), safety data in patients with liver disease is limited to preclinical studies. Always discuss with your physician before using any peptide if you have a liver condition.

Which peptide has the strongest evidence for liver health?

For human clinical evidence, semaglutide leads the field. The phase 2 NEJM trial showed NASH resolution in 59% of patients. For preclinical evidence, BPC-157 has the longest track record, with studies spanning over 30 years across multiple liver injury models.

Can you combine liver-protective peptides?

There is limited research on peptide combinations for liver health specifically. However, the peptides covered here work through different mechanisms (anti-inflammatory, anti-fibrotic, metabolic), so there is theoretical rationale for complementary effects. See our peptide stacking guide for general principles on combining peptides.

Do peptides cause liver damage?

GLP-1 receptor agonists have been extensively studied and do not appear to cause liver damage. BPC-157 is metabolized in the liver with a half-life of less than 30 minutes — preclinical studies show no hepatotoxicity. However, contaminated or low-quality peptide products could potentially cause harm, which is why sourcing and purity are important considerations.

What about food-derived hepatoprotective peptides?

There is a growing body of research on bioactive peptides from natural food sources — including soy, wheat, marine organisms, and bovine casein — that show hepatoprotective properties in preclinical models. These peptides typically work through antioxidant activity and lipid metabolism regulation. One example is PGPIPN, a hexapeptide from bovine beta-casein that reduced alcoholic fatty liver disease markers in mice.

The Bottom Line

Peptide research for liver health spans a wide range of compounds and evidence levels. GLP-1 receptor agonists like semaglutide stand out with the strongest human clinical evidence — they're FDA-approved, physician-prescribed, and backed by rigorous trials showing meaningful improvement in fatty liver disease. BPC-157 has the deepest preclinical track record, with over 30 years of animal studies demonstrating consistent hepatoprotective effects across multiple injury models. TB-500 and GHK-Cu offer promising anti-fibrotic data, and KPV addresses the increasingly recognized gut-liver axis.

The field is moving fast. New peptide compounds like S6-FA (a novel anti-fibrotic peptide published in 2025) and next-generation multi-agonists (retatrutide, survodutide) are expanding what's possible. But the fundamentals haven't changed: liver health still starts with diet, weight management, limiting alcohol, and working with a physician who can monitor your liver function and guide treatment decisions.

If you're interested in peptides that support related areas, explore our guides on best peptides for inflammation, best peptides for gut health, and best peptides for anti-aging and longevity.

References

  1. Turkovic B, et al. "Hepatoprotective effect of BPC 157, a 15-amino acid peptide, on liver lesions induced by either restraint stress or bile duct and hepatic artery ligation or CCl4 administration." Life Sciences. 1993;53(18):PL291-6. PubMed

  2. Chang CH, et al. "Pentadecapeptide BPC 157 efficiently reduces radiation-induced liver injury and lipid accumulation through Kruppel-like factor 4 upregulation both in vivo and in vitro." Life Sciences. 2022;310:121079. PubMed

  3. Bilge SS, et al. "Protective Effects of BPC 157 on Liver, Kidney, and Lung Distant Organ Damage in Rats with Experimental Lower-Extremity Ischemia-Reperfusion Injury." Medicina. 2025;61(2):291. PMC

  4. Sikiric P, et al. "The pharmacological properties of the novel peptide BPC 157 (PL-10)." Inflammopharmacology. 1999;7(1):1-14. Springer

  5. Newsome PN, et al. "A Placebo-Controlled Trial of Subcutaneous Semaglutide in Nonalcoholic Steatohepatitis." New England Journal of Medicine. 2021;384(12):1113-1124. NEJM

  6. Flint A, et al. "Once-Weekly Subcutaneous Semaglutide Improves Fatty Liver Disease in Patients with Type 2 Diabetes: A 52-Week Prospective Real-Life Study." Nutrients. 2022;14(21):4673. PMC

  7. Loomba R, et al. "Semaglutide 2.4 mg once weekly in patients with non-alcoholic steatohepatitis-related cirrhosis." The Lancet Gastroenterology & Hepatology. 2023;8(6):511-522. The Lancet

  8. Shah R, et al. "Thymosin beta 4 prevents oxidative stress, inflammation, and fibrosis in ethanol-induced liver injury in mice." International Journal of Molecular Sciences. 2018. PubMed

  9. Kim J, et al. "Exogenous thymosin beta 4 prevents CCl4-induced acute liver injury and subsequent fibrosis." Research article. 2015.

  10. Zuo Y, et al. "Thymosin beta-4 prevents hepatocyte apoptosis by reversing lincRNA-p21-mediated caspase activation." Research article.

  11. Kim J, et al. "Hepatic stellate cells express thymosin beta 4 in chronically damaged liver." PLoS ONE. 2015.

  12. Pickart L, Thaler MM. "A synthetic tripeptide which increases survival of normal liver cells, and stimulates growth in hepatoma cells." Biochemical and Biophysical Research Communications. 1973;54(2):562-566. ScienceDirect

  13. Pickart L, Margolina A. "Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data." International Journal of Molecular Sciences. 2018;19(7):1987. PMC

  14. Dou Y, et al. "The potential of GHK as an anti-aging peptide." Aging Pathobiology and Therapeutics. 2020;2(1):58-61. APT

  15. Pickart L. "The human tripeptide GHK-Cu in prevention of oxidative stress and degenerative conditions of aging." Oxidative Medicine and Cellular Longevity. 2012.

  16. Dalmasso G, et al. "PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation." Gastroenterology. 2008;134(1):166-178. PMC

  17. Lee C, et al. "Humanin treatment of human hepatocytes results in decreased lipid accumulation." Frontiers in Endocrinology. 2021. Frontiers

  18. Muzumdar RH, et al. "Humanin: A novel central regulator of peripheral insulin action." PLoS ONE. 2009.