Best Peptides for Kidney Health

Your kidneys filter about 45 gallons of blood every day. They remove waste products, balance electrolytes, regulate blood pressure, and produce hormones that control red blood cell production. When kidney function declines, everything downstream suffers — from bone health to cardiovascular risk.

Chronic kidney disease (CKD) affects roughly 37 million Americans, and most don't know they have it until significant function is already lost. Acute kidney injury (AKI) — a sudden drop in kidney function from surgery, sepsis, or medication toxicity — remains one of the most challenging conditions in critical care medicine. There are currently no drugs specifically approved to treat AKI.

That's why peptide-based kidney therapies are a growing area of research. From GLP-1 agonists that recently earned FDA approval for CKD to experimental peptides targeting renal fibrosis at the molecular level, this guide covers what the current science says about peptides and kidney health.

How Kidneys Get Damaged — and Why Fibrosis Is the Central Problem
Semaglutide: FDA-Approved Kidney Protection (The FLOW Trial)
BPC-157: Multi-Organ Protection Including the Kidneys
Thymosin Beta-4 and Ac-SDKP: The Anti-Fibrotic Duo
GHK-Cu: Preferential Kidney Accumulation
KP1: A Klotho-Derived Anti-Fibrotic Peptide
Humanin and MOTS-c: Mitochondrial Peptides in CKD
Emerging Peptide Therapies for Kidney Disease
Peptide Comparison Table
Important Caveats
Frequently Asked Questions
The Bottom Line
References

How Kidneys Get Damaged — and Why Fibrosis Is the Central Problem

Kidney damage follows a common pathway regardless of the initial cause — whether it's diabetes, high blood pressure, drug toxicity, or ischemia. Understanding this pathway explains why so many peptide therapies target the same set of mechanisms.

The damage progression:

Initial injury — Tubular cells, podocytes, or glomerular endothelial cells are damaged by the triggering insult
Inflammatory response — Macrophages and other immune cells accumulate, releasing TNF-alpha, IL-1-beta, IL-6, and MCP-1
Oxidative stress — Reactive oxygen species overwhelm the kidney's antioxidant defenses
TGF-beta activation — This is the master switch. Transforming growth factor beta-1 (TGF-beta-1) activates the Smad signaling cascade
Myofibroblast formation — Normal kidney cells transform into collagen-producing myofibroblasts through a process called epithelial-to-mesenchymal transition
Fibrosis — Scar tissue replaces functional kidney tissue, reducing filtration capacity

Once fibrosis becomes established, kidney function decline becomes progressive and largely irreversible. That's why the most promising peptide therapies focus on interrupting this cascade — particularly the TGF-beta/Smad pathway — before permanent scarring sets in.

Semaglutide: FDA-Approved Kidney Protection (The FLOW Trial)

Semaglutide is the first GLP-1 receptor agonist with dedicated kidney outcomes data from a major clinical trial. In January 2025, the FDA approved semaglutide (Ozempic) for reducing kidney disease progression in patients with type 2 diabetes and CKD.

The FLOW Trial

The FLOW trial was a double-blind, randomized, placebo-controlled study of 3,533 patients with type 2 diabetes and chronic kidney disease. It compared once-weekly injectable semaglutide (1.0 mg) to placebo on top of standard care [1].

The trial was stopped early because the results were so clear.

Key results:

24% reduction in the primary composite endpoint (kidney failure, substantial loss of kidney function, death from kidney or cardiovascular causes)
Slowed eGFR decline by 1.16 mL/min/1.73 m-squared per year — a clinically meaningful preservation of kidney function
18% reduction in three-point major adverse cardiovascular events (MACE)
20% reduction in all-cause mortality

The patient population was high-risk: 93% had high or very high-risk CKD by KDIGO criteria, and about 95% were already receiving standard RAAS blockade therapy.

A "Fourth Pillar" of CKD Treatment

Based on the FLOW results, the American Diabetes Association updated its guidelines to recommend GLP-1 receptor agonists as a treatment for type 2 diabetes with CKD. Semaglutide now joins RAAS blockers, SGLT2 inhibitors, and finerenone as the four pillars of CKD management in diabetes [2].

Modeling studies estimate that combination therapy with all four classes could improve event-free survival by 5.5 years for CKD progression, 3.2 years for cardiovascular events, and 2.4 years for all-cause mortality — compared to RAAS blockade alone.

How Semaglutide Protects Kidneys

Lowers blood sugar — Reducing glucose-mediated damage to glomerular filtering units
Reduces proteinuria — Less protein in the urine means less tubular damage
Weight loss — Reduces metabolic stress on the kidneys
Anti-inflammatory effects — Decreases kidney scarring and inflammation
Blood pressure reduction — Lowers mechanical stress on glomeruli
GLP-1 receptors in the kidney — Animal studies show that genetic deletion of GLP-1 receptors causes albuminuria and glomerulosclerosis, suggesting a direct renal protective role [3]

Tirzepatide, a dual GIP/GLP-1 agonist, is also being studied for kidney outcomes and may offer additional benefits through its dual mechanism.

BPC-157: Multi-Organ Protection Including the Kidneys

BPC-157 (Body Protection Compound-157) has been studied primarily for gastrointestinal and musculoskeletal healing, but emerging research shows notable kidney-protective effects — and the peptide naturally accumulates in renal tissue at high concentrations.

Pharmacokinetic Evidence: BPC-157 Goes to the Kidneys

This is one of the more intriguing findings. Pharmacokinetic studies show that after administration, BPC-157 concentrates preferentially in kidney tissue. Within 10 minutes, the mean renal tissue concentration reached 223 ng equivalent per mL — higher than the plasma concentration of 150 ng equivalent per mL. After one hour, the average kidney concentration peaked at 560 ng equivalent per mL, the highest of any tissue measured, followed by liver, stomach wall, spleen, and thymus [4].

This natural affinity for kidney tissue suggests the kidneys may be an important target organ for BPC-157's biological effects.

Ischemia-Reperfusion Protection (2025)

A 2025 study published in Medicina tested BPC-157 in rats with lower-extremity ischemia-reperfusion injury, evaluating its effects on distant organ damage to the kidneys, liver, and lungs [5].

In the kidneys, BPC-157 significantly reduced:

Vascular and glomerular vacuolization
Tubular dilation
Hyaline cast formation
Tubular cell shedding

The BPC-157 treatment group showed statistically significant increases in total antioxidant status (TAS) and paraoxonase-1 (PON-1) activity in renal tissue, with reduced total oxidant status (TOS) and oxidative stress index (OSI).

Hydronephrosis Recovery (2020)

A study presented at FASEB examined BPC-157 in rats with hydronephrosis caused by 72 hours of ureteral ligation. After the obstruction was removed, BPC-157 was administered at doses of 10 micrograms per kg or 10 nanograms per kg [6].

The results were striking. Severe hydronephrosis — with dilated renal pelvis and thinned parenchyma — was reversed to mild or no hydronephrosis within 24 to 96 hours. The peptide also reduced fibrosis development, tubular cell damage, and interstitial inflammation.

Mechanisms in the Kidney

BPC-157's renal protective effects appear to work through:

Antioxidant enzyme upregulation — Increased expression of heme oxygenase-1 (HO-1) and heat shock proteins (HSP70 and HSP90)
Anti-inflammatory action — Reduced pro-inflammatory cytokine release
Anti-fibrotic effects — Inhibition of TGF-beta pathways and collagen deposition
Anti-apoptotic mechanisms — Protection of podocytes and endothelial cells from programmed cell death

For the full research profile, see our BPC-157 complete guide.

Thymosin Beta-4 and Ac-SDKP: The Anti-Fibrotic Duo

TB-500 is a synthetic fragment of thymosin beta-4 (Tβ4), a 43-amino acid peptide present in nearly all mammalian cells. For kidney disease specifically, the story centers on both the parent peptide and its degradation product, Ac-SDKP — a tetrapeptide that has become one of the most studied anti-fibrotic compounds in nephrology.

The Tβ4-POP-Ac-SDKP Axis

Here's how it works: Thymosin beta-4 is broken down in the body by prolyl oligopeptidase (POP) into Ac-SDKP (N-acetyl-seryl-aspartyl-lysyl-proline). Ac-SDKP is then inactivated by angiotensin-converting enzyme (ACE). This means ACE inhibitors — one of the most commonly prescribed drugs for kidney disease — may work partly by preventing Ac-SDKP from being degraded, keeping protective levels higher [7].

This connection between ACE inhibitors and Ac-SDKP is not just theoretical. Research has shown that a monoclonal antibody blocking Ac-SDKP eliminated the anti-fibrotic and anti-inflammatory effects of the ACE inhibitor captopril — without affecting blood pressure or cardiac hypertrophy. In other words, some of the kidney-protective benefits of ACE inhibitors may come from their preservation of endogenous Ac-SDKP levels [8].

Ac-SDKP in Kidney Fibrosis Models

The anti-fibrotic effects of Ac-SDKP in the kidney have been demonstrated across multiple experimental models:

Reduced collagen and fibronectin deposition in fibrosis models
Fewer myofibroblasts and macrophages in damaged kidney tissue
Suppressed TGF-beta signaling — specifically reduced Smad2 phosphorylation and increased Smad7 expression
Reduced pro-inflammatory gene expression — ICAM-1, IL-1-beta, MCP-1, and TNF-alpha were all lowered
Effective in both early and late stages of kidney injury [9]

Diabetic Nephropathy

In diabetic rats, Ac-SDKP administration significantly reduced renal fibrosis. When combined with the ACE inhibitor ramipril, fibrosis reduction exceeded what either treatment achieved alone — suggesting an additive benefit [10].

The Nuance: Tβ4 Is Not Simple

One important finding: Tβ4 by itself has a complex relationship with fibrosis. When combined with a POP inhibitor (which blocks Ac-SDKP production), thymosin beta-4 actually promoted fibrosis. But when given alone, Tβ4 had anti-fibrotic effects in late-stage disease — because POP was free to convert it to the anti-fibrotic Ac-SDKP [9]. The bottom line: the protective effects depend on the availability of Ac-SDKP, not thymosin beta-4 alone.

For more on TB-500 research, see our TB-500 mechanisms guide.

GHK-Cu: Preferential Kidney Accumulation

GHK-Cu (glycyl-L-histidyl-L-lysine copper complex) is best known for skin and wound healing research, but it has several properties relevant to kidney health — starting with where it goes in the body.

It Accumulates in the Kidneys

When tritiated (radiolabeled) copper-free GHK was injected intravenously into mice, it concentrated most densely in the kidneys and brain after 4 hours [11]. This preferential accumulation suggests the kidneys may be a significant target organ for GHK's biological activity.

Anti-Fibrotic Mechanisms

GHK-Cu's most relevant kidney action involves its effect on renal fibrosis drivers:

Decorin upregulation: GHK-Cu stimulates production of decorin, an anti-inflammatory proteoglycan that can protect against kidney-damaging fibrosis in diabetic models. Decorin is known to regulate TGF-beta signaling — the master switch in renal fibrogenesis [12].
TGF-beta-1 suppression: GHK-Cu downregulates TGF-beta-1 expression, potentially interrupting the key signaling cascade that drives collagen deposition in the kidney [13].
Antioxidant activity: At concentrations as low as 10 micromolar, GHK reduces reactive oxygen species by nearly 50% in cell models, with hydroxyl radical quenching activity stronger than glutathione [14].
Anti-inflammatory effects: Suppresses NFkB signaling, TNF-alpha, and IL-6 — all contributors to renal inflammation.

GHK serum levels drop from about 200 ng/mL at age 20 to 80 ng/mL by age 60. Since CKD risk increases with age, and GHK has anti-fibrotic properties that target key renal fibrosis pathways, this decline may be relevant to age-related kidney disease susceptibility [15].

The kidney-specific research on GHK-Cu remains early-stage, but the combination of preferential renal accumulation, TGF-beta suppression, and decorin production makes it an interesting candidate for further study. See our GHK-Cu science guide for the full research profile.

KP1: A Klotho-Derived Anti-Fibrotic Peptide

KP1 is a 30-amino acid peptide derived from klotho — a protein strongly associated with kidney health and aging. Klotho is predominantly produced in the kidneys, and its decline is linked to CKD progression and accelerated aging.

Mechanism of Action

KP1 works by binding directly to the type 2 TGF-beta receptor (TβR2), disrupting TGF-beta-1 signaling and inhibiting myofibroblast activation — the process that converts normal kidney cells into scar-producing cells [16].

Animal Study Results

In mouse models, KP1 demonstrated:

Reduced kidney fibrosis in both ischemia-reperfusion and obstructive uropathy models
Preserved kidney function as measured by standard biomarkers
Preferential kidney targeting — KP1 primarily accumulated in injured kidneys following intravenous injection

Practical Advantages

Researchers have noted that peptides like KP1 are relatively easy and inexpensive to synthesize, have low inherent toxicity, and no safety concerns were detected in KP1-injected mice. This makes them attractive candidates for potential CKD therapy development [16].

KP1 is still in the preclinical stage, but it represents a targeted approach — using a fragment of the kidney's own protective protein to combat the specific mechanism (TGF-beta signaling) that drives renal fibrosis.

Humanin and MOTS-c: Mitochondrial Peptides in CKD

Humanin and MOTS-c are mitochondrial-derived peptides (MDPs) — short peptides encoded directly by mitochondrial DNA. Both have been measured in kidney tissue and linked to kidney disease outcomes.

Humanin in CKD

Humanin is a 24-amino acid peptide with anti-apoptotic and cytoprotective properties. In the context of kidney disease:

Elevated circulating levels in CKD: Patients with chronic kidney disease have higher plasma humanin levels compared to healthy controls — interpreted as a hormetic stress response, meaning the body ramps up production in an attempt to protect against ongoing damage [17].
Reduced muscle expression: While circulating levels go up in CKD, humanin expression in skeletal muscle goes down. Researchers believe this means production shifts to other sites — potentially the liver, endothelial cells, or the kidneys themselves.
Anti-apoptotic protection: Humanin protects cells from oxidative stress-induced death, which is directly relevant to tubular cell survival during kidney injury.

MOTS-c in CKD

MOTS-c is a 16-amino acid mitochondrial peptide that functions as a metabolic regulator. It is expressed in multiple organs including the kidneys and circulating plasma.

Reduced in CKD: Unlike humanin, MOTS-c levels are reduced in both skeletal muscle and serum in patients with CKD [17].
Metabolic regulation: MOTS-c activates AMPK, inhibits de novo purine synthesis, and regulates fatty acid metabolism — pathways relevant to the metabolic stress that drives CKD progression.
Mitochondrial dysfunction connection: Mitochondrial dysfunction is a proposed major contributor to poor kidney function and muscle wasting in CKD. The decline of protective MDPs like MOTS-c may both reflect and accelerate this dysfunction.

The Bigger Picture

The discovery that mitochondria produce their own signaling peptides — and that these peptides decline in kidney disease — opens a new angle on renal protection. It suggests that supporting mitochondrial health may be important for kidney function, and that restoring MDP levels could potentially slow disease progression. However, therapeutic applications are still in early preclinical investigation.

For more on mitochondrial peptides, see our guides on humanin, MOTS-c, and SS-31.

Emerging Peptide Therapies for Kidney Disease

Several newer peptide-based approaches are worth mentioning, even though they are in earlier stages of development:

PEP-Z-2 (Collagen Peptide for Renal Fibrosis)

PEP-Z-2 is a collagen peptide isolated from redlip croaker (a fish) scales. In mouse models, it alleviated kidney injury induced by both unilateral ureteral obstruction (UUO) and folic acid, reduced collagen deposition, normalized renal function, and restored oxidant/antioxidant balance. It works through the TGF-beta/Smad/AKT/MAPK signaling pathway [18].

TIP Peptide (For Nephritis)

The TIP peptide takes a creative approach to kidney protection. Rather than broadly suppressing TNF (which would impair immune defense against infections), TIP selectively counteracts TNF's harmful effects in the kidney — restoring prostaglandin E2 and nitric oxide levels that protect against nephrotoxic nephritis [19].

AI-Designed Kidney-Targeting Peptides

A 2025 study published in Science Advances used AlphaFold to design a library of 1,885 peptides targeting KIM1 (kidney injury molecule-1), a protein that is markedly upregulated in injured kidneys but barely expressed in healthy ones. The best-performing peptide, TKP4, efficiently targeted injured renal cells. When loaded onto liposomes with the drug nystatin, TKP4-decorated particles targeted injured mouse kidneys and reduced AKI severity [20].

This represents a shift toward precision kidney medicine — using AI and molecular targeting to deliver therapies specifically to damaged kidney cells while sparing healthy tissue.

Peptide Comparison Table

Peptide	Primary Kidney Mechanism	Research Stage	Key Evidence	Clinical Application
Semaglutide	Metabolic protection, anti-inflammatory, direct renal GLP-1R effects	Phase 3 (FLOW trial) / FDA-approved	24% reduction in major kidney events; trial stopped early for efficacy	FDA-approved for CKD in T2D
BPC-157	Antioxidant, anti-inflammatory, natural kidney accumulation	Preclinical (animal studies)	Reversed hydronephrosis; protected against I/R kidney injury	Not FDA-approved
Ac-SDKP (TB4 fragment)	Anti-fibrotic, TGF-beta/Smad inhibition	Preclinical (animal studies)	Reduced fibrosis in multiple kidney models; additive to ACE inhibitors	Not FDA-approved
GHK-Cu	Decorin upregulation, TGF-beta suppression, preferential kidney targeting	Preclinical (in vitro + animal)	Accumulates in kidneys; upregulates anti-fibrotic decorin	Not FDA-approved
KP1	Direct TGF-beta receptor blockade	Preclinical (animal studies)	Reduced fibrosis and preserved function in two kidney injury models	Not FDA-approved
Humanin	Anti-apoptotic, cytoprotective	Preclinical (observational + animal)	Elevated in CKD patients (stress response); anti-apoptotic in cell models	Not FDA-approved
MOTS-c	Metabolic regulation via AMPK	Preclinical (observational + animal)	Reduced in CKD; associated with mitochondrial dysfunction	Not FDA-approved
TKP4	Targeted drug delivery to injured kidney cells	Preclinical (animal + AI design)	AI-designed; targeted injured kidneys via KIM1 binding	Experimental

Important Caveats

Semaglutide is the only FDA-approved option. The FLOW trial data led to regulatory approval for CKD in type 2 diabetes. Every other peptide on this list is investigational for kidney disease.

Preclinical results don't guarantee human efficacy. Animal models of kidney disease — particularly rodent UUO and ischemia-reperfusion models — are useful but imperfect. Many promising preclinical therapies fail in human trials.

CKD requires medical management. If you have chronic kidney disease, work with a nephrologist. Standard therapies (RAAS blockers, SGLT2 inhibitors, finerenone, semaglutide) have strong clinical evidence and should form the foundation of treatment.

Kidney-toxic contaminants are a real risk. Non-FDA-approved peptides vary in quality. Products contaminated with heavy metals, endotoxins, or solvents can directly damage the kidneys — the very organ you're trying to protect. This matters more for kidney health than almost any other application.

The four-pillar approach. For patients with type 2 diabetes and CKD, the current evidence supports combining RAAS blockade, SGLT2 inhibitors, finerenone, and GLP-1 receptor agonists. This combination approach has the strongest evidence for preserving kidney function.

Frequently Asked Questions

Can peptides reverse kidney damage?

The kidney has some regenerative capacity, but it's much more limited than the liver's. Early-stage fibrosis may be partially reversible if the underlying cause is controlled. In animal models, peptides like Ac-SDKP and BPC-157 have reduced established fibrosis markers. However, advanced CKD with widespread scarring is generally considered irreversible. The realistic goal with most peptide therapies is slowing progression, not reversal.

Which peptide has the strongest evidence for kidney health?

Semaglutide, by a wide margin. The FLOW trial — a large, randomized, placebo-controlled trial with 3,533 patients — demonstrated a 24% reduction in major kidney disease events. No other peptide has this level of clinical evidence for kidney outcomes.

Do peptides cause kidney damage?

GLP-1 receptor agonists have been studied extensively and do not appear to damage the kidneys — in fact, they protect them. BPC-157 pharmacokinetic studies show it accumulates naturally in kidney tissue with no reported nephrotoxicity in preclinical studies. However, poorly manufactured or contaminated peptide products can contain nephrotoxic substances. Sourcing from reputable manufacturers and monitoring kidney function with your physician is important.

How does the gut affect kidney health, and do gut peptides help?

The gut-kidney axis is a recognized concept in nephrology. Intestinal barrier dysfunction allows uremic toxins and inflammatory mediators to enter circulation, worsening CKD progression. Peptides that support gut health — like KPV and BPC-157 — may indirectly benefit kidney health by reducing this inflammatory burden. See our best peptides for gut health guide for more.

Can you combine kidney-protective peptides?

For FDA-approved therapies, yes — the evidence actually supports combination. Semaglutide with SGLT2 inhibitors and RAAS blockers appears to have additive kidney benefits. For non-FDA-approved peptides, combination data is minimal. See our peptide stacking guide for general principles.

What about peptides for acute kidney injury (AKI)?

AKI remains one of the biggest unmet needs in nephrology — there are no approved drugs specifically for it. BPC-157 has shown protection against ischemia-reperfusion kidney injury in animal models, and the AI-designed TKP4 peptide specifically targets injured kidney cells. These are promising leads, but both are still preclinical.

The Bottom Line

Peptide therapy for kidney health has changed dramatically with the FLOW trial results. Semaglutide is now a proven, FDA-approved kidney-protective agent for patients with type 2 diabetes and CKD — reducing major kidney events by 24% and earning a place as the "fourth pillar" of CKD management alongside RAAS blockers, SGLT2 inhibitors, and finerenone.

Beyond semaglutide, the preclinical pipeline is rich. BPC-157's natural kidney accumulation and multi-mechanism protection, Ac-SDKP's potent anti-fibrotic effects (which may explain some benefits of ACE inhibitors), and GHK-Cu's preferential kidney targeting all represent promising research directions. Newer approaches — klotho-derived peptides, AI-designed kidney-targeting compounds, and mitochondrial-derived peptides — show that the field is moving toward precision therapies.

But the fundamentals remain the same: blood pressure control, blood sugar management, maintaining a healthy weight, staying hydrated, avoiding nephrotoxic substances, and working with a nephrologist if you have CKD. Peptides may add to this foundation. They don't replace it.

For related research, see our guides on best peptides for cardiovascular health, best peptides for inflammation, and best peptides for anti-aging and longevity.

References

Perkovic V, et al. "Effects of Semaglutide on Chronic Kidney Disease in Patients with Type 2 Diabetes." New England Journal of Medicine. 2024. NEJM
American Diabetes Association. "Semaglutide Reduced Risk for Major Kidney Disease Events by 24% for Patients with Type 2 Diabetes and Kidney Disease." Press release, 2024. ADA
Tuttle KR, et al. "Glucagon-like Peptide-1 Receptor Agonists: New Evidence of Kidney and Cardiovascular Protection From the FLOW and SELECT Trials." American Journal of Kidney Diseases. 2024. AJKD
Chang CH, et al. "Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157 in rats and dogs." Frontiers in Pharmacology. 2022;13:1026182. Frontiers
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
Vranes H, et al. "In Hydronephrosis-Rats, BPC 157 Exerts a Strong Anti-Ulcer Effect in Both Stomach and Duodenum along with Marked Kidney Recovery." The FASEB Journal. 2020;34(S1):03972. FASEB
Kanasaki K, et al. "The Role of Tβ4-POP-Ac-SDKP Axis in Organ Fibrosis." International Journal of Molecular Sciences. 2022;23(21):13282. MDPI
Peng H, et al. "Tβ4-Ac-SDKP pathway: Any relevance for the cardiovascular system?" Pharmacological Research. 2019;150:104509. PMC
Zuo Y, et al. "Thymosin β4 and its degradation product, Ac-SDKP, are novel reparative factors in renal fibrosis." Kidney International. 2013;84(6):1166-1175. PMC
Castoldi G, et al. "Ac-SDKP administration reduces renal fibrosis in diabetic nephropathy." Nephrology Dialysis Transplantation. 2010.
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
Pickart L. "The human tripeptide GHK-Cu in prevention of oxidative stress and degenerative conditions of aging." Oxidative Medicine and Cellular Longevity. 2012.
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
Dou Y, et al. "The potential of GHK as an anti-aging peptide." Aging Pathobiology and Therapeutics. 2020;2(1):58-61. APT
Pickart L. "GHK serum levels decline with age." Multiple publications. 1973-2018.
Yuan Q, et al. "A Klotho-Derived Peptide as a Possible Novel Drug to Prevent Kidney Fibrosis." American Journal of Kidney Diseases. 2022;80(6):e25-e27. AJKD
Peng T, et al. "Reduced skeletal muscle expression of mitochondrial-derived peptides humanin and MOTS-C and Nrf2 in chronic kidney disease." American Journal of Physiology-Renal Physiology. 2019;317(5):F1122-F1131. APS
Li X, et al. "The novel peptide PEP-Z-2 potentially treats renal fibrosis in vivo and in vitro by regulating TGF-β/Smad/AKT/MAPK signaling." European Journal of Pharmacology. 2024;964:176319. ScienceDirect
"Peptide shows promise for protecting kidneys from nephritis." ScienceDaily. March 25, 2019. ScienceDaily
Liu S, et al. "A rationally designed injury kidney targeting peptide library and its application in rescuing acute kidney injury." Science Advances. 2025. Science

Table of Contents