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Free U.S. shipping on orders over $150Sermorelin is a synthetic analog of growth hormone–releasing hormone (GHRH). GHRH is a naturally occurring peptide secreted by the hypothalamus to stimulate growth hormone (GH) production in the anterior pituitary gland.
Structurally, sermorelin is a 29–amino acid peptide fragment of GHRH that retains full biological activity in terms of binding to pituitary receptors and triggering GH release [1].
Originally, sermorelin was developed as a diagnostic tool to assess pituitary function. Over time, its use has expanded into research exploring potential roles as a secretagogue in endocrine regulation, metabolism, and aging biology.
Sermorelin stimulates the pituitary to produce and secrete GH, which in turn drives the liver and peripheral tissues to generate insulin-like growth factor-1 (IGF-1), the primary mediator of bone elongation and linear growth.
Clinical trials in children with impaired growth velocity have shown that sermorelin administration can increase growth rate and promote catch-up growth.
Specifically, once-daily subcutaneous Sermorelin (30 µg/kg body weight) at bedtime was effective in treatment of prepubertal children with idiopathic GH deficiency [2].
Although sermorelin-treated children demonstrated less height improvements compared to 30 µg/kg/day of somatropin (bioidentical GH), sermorelin was likely safer and better tolerated.
Unlike direct GH therapy, sermorelin does not appear to excessively elevate circulating GH or IGF-1 levels, potentially lowering the risk of disproportionate bone growth or metabolic complications.
In this context, sermorelin is best understood as a diagnostic and therapeutic tool that can support normal developmental trajectories in children with specific types of growth impairment.
However, long-term data remain limited, and not all forms of growth delay respond equally, underscoring the importance of careful patient selection in research and clinical settings.
Preclinical studies suggest that GHRH analogs similar to sermorelin can exert anti-proliferative effects in certain cancer models. Mechanistically, these peptides appear to influence signaling pathways that regulate apoptosis, angiogenesis, and cell cycle progression [3].
A transcriptomic screen for candidate compounds in treatment-resistant glioma patients identified sermorelin as a candidate compound effective against the glioma [4].
Among screened compounds, sermorelin emerged as the most promising agent for recurrent gliomas, especially those with high-grade tumors, IDH-wildtype status, and 1p/19q non-codeletion.
This study suggests that sermorelin may inhibit glioma cell proliferation by blocking the cell cycle, although clinical validation is required.
GH and IGF-1 support osteoblast activity, increase bone turnover, and may help reverse age‐related loss of bone mass. These hormones also support muscle growth and maintenance along with tissue repair [5, 6]. As a GH secretagogue, sermorelin may mitigate some aspects of age-related decline in bone health. However, specific trials of sermorelin in aging adults focused on bone density remain limited.
A single-blind, randomized, placebo-controlled trial of 19 people investigated the effects of nightly subcutaneous sermorelin at 10 µg/kg for 16 weeks. Results showed [7]:
While body weight, fat mass, and testosterone levels remained stable, these findings suggest sermorelin may mitigate age-related GH/IGF-1 decline and corresponding muscle mass loss.
In clinical and research use, sermorelin has generally been regarded as safe and well tolerated, especially in comparison to direct recombinant growth hormone therapy.
Because it acts as a secretagogue, stimulating the body’s own pulsatile growth hormone release rather than providing supraphysiologic doses, its endocrine profile is considered closer to natural physiology.
The most frequently reported adverse effects are mild and transient, such as injection site reactions, flushing sensation, and nausea.
Serious side effects are rare in published reports, and no consistent evidence suggests long-term harm at research dosages.
However, as with other growth hormone-modulating therapies, caution is advised in individuals with active malignancy, since GH and IGF-1 pathways can influence cell proliferation.
Overall, the safety data indicate a favorable risk profile for sermorelin within short- to medium-term use, though robust long-term clinical studies are limited.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Sermorelin is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 6-panel testing protocol: identification by ESI-MS, purification by RP-HPLC, conformity, sterility screening, quantification of net peptide content, and LAL endotoxin screening. Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
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No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and quantification data where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 100+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.
Summary Sermorelin + GHRP-6 + GHRP-2 combines complementary upstream signals within the growth hormone axis. Sermorelin activates GH synthesis through the GHRH receptor, while GHRP-6 and GHRP-2 stimulate the ghrelin receptor GHS-R1a to amplify GH pulse release. Together, they enhance endogenous, pulsatile growth hormone signaling through dual-pathway stimulation, along with some gastric ghrelin effects. What Is Sermorelin? Sermorelin is a synthetic 29-amino acid fragment of growth hormone–releasing hormone [1]. It represents the shortest, completely functional portion of the endogenous GHRH. Sermorelin works via upstream mechanisms rather than supplying growth hormone directly [1]. It acts through the GHRH receptor on somatotroph cells in the anterior pituitary to increase growth hormone synthesis and pulsatile secretion [2]. Sermorelin remains under normal physiologic regulation through negative feedback from somatostatin, which helps modulate growth hormone output and preserve its natural pulsatile release pattern [2]. In addition to stimulating secretion, sermorelin also supports transcription of the growth hormone gene, helping to maintain the integrity of the growth hormone neuroendocrine axis [3]. Because it stimulates endogenous growth hormone production rather than replacing growth hormone directly, sermorelin is considered a more physiologic approach to enhancing growth hormone signalling [3]. What Is GHRP-2? Growth hormone–releasing peptide-2 (GHRP-2), is a synthetic hexapeptide that functions as a growth hormone secretagogue [4]. It agonises ghrelin receptor GHS-R1a, a G-protein-coupled receptor expressed in the hypothalamus and anterior pituitary [4]. When GHRP-2 binds GHS-R1a, intracellular signalling pathways activate, increasing calcium flux and downstream second-messenger activity to stimulate pulsatile growth hormone release from pituitary somatotroph cells [5]. GHS-R1a receptor activation also increases the amplitude of growth hormone pulses and can raise circulating Insulin-like Growth Factor (IGF-1) [6]. In addition to growth hormone, GHRP-2 may stimulate adrenocorticotropic hormone (ACTH), suggesting broader HPA-axis engagement [7]. Because it works via receptor-mediated stimulation rather than direct hormone replacement, GHRP-2 is widely used in research and in diagnostics to assess growth hormone reserve [8]. Its unique pharmacologic profile makes it a tool for studying ghrelin receptor signalling, endocrine feedback regulation, and somatotrophic axis dynamics [7]. What Is GHRP-6? Growth hormone–releasing peptide-6 (GHRP-6) is a synthetic hexapeptide that also functions as a growth hormone secretagogue [9]. Like GHRP-2, GHRP-6 acts as an agonist of the G-protein-coupled ghrelin receptor GHS-R1a, expressed in the hypothalamus and anterior pituitary [9]. This binding mimics the action of endogenous ghrelin and stimulates intracellular signalling cascades that increase calcium mobilization and promote pulsatile growth hormone release from pituitary somatotroph cells [10]. This mechanism enhances both the amplitude and frequency of growth hormone pulses [10]. The effects of GHRP-6 appear to be influenced by metabolic context, with insulin augmenting the growth hormone response, while concurrent carbohydrate or lipid intake can blunt it [11]. Interestingly, GHRP-6 is one of the only GHRPs that can actively increase hunger and food intake. Because it stimulates endogenous growth hormone release via receptor activation rather than direct hormone administration, GHRP-6 is primarily used in research contexts to study ghrelin signalling, somatotropic regulation, and downstream metabolic effects [11]. Sermorelin, GHRP-2, and GHRP-6 Synergy The combination of sermorelin with growth hormone–releasing peptides produce complementary effects through stimulation of growth hormone release via two unique upstream receptors that converge on the same pituitary somatotroph output [12]. Sermorelin activates the GHRH receptor to promote growth hormone synthesis and physiologic, pulsatile secretion [2]. Conversely, GHRP-2 and GHRP-6 act as ghrelin receptor agonists, which increase intracellular signalling and calcium-dependent pathways that also drive pulsatile growth hormone release [5,10]. Pairing a GHRH-pathway signal from sermorelin with a ghrelin pathway signal from GHRPs may produce a stronger growth hormone pulse than either agent alone through stimulating the axis from two distinct areas rather than one. Dosage and Balance Considerations There is some in vitro evidence to suggest that GHRP-2 and GHRP-6 each act synergistically with GHRH to stimulate growth hormone release, supporting the rationale for combining a GHRH analogue like sermorelin with a GHRP [12]. Equal dosing in this formulation is designed to provide a balanced stimulation across both regulatory arms of the somatotropic axis to support a coordinated GH pulse rather than disproportionally driving one pathway. References: 1 Prakash, A. and Goa, K. L. (1999) Sermorelin: A review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency. BioDrugs, Springer Nature 12, 139–157 2 Ishida, J., Saitoh, M., Ebner, N., Springer, J., Anker, S. D. and von Haehling, S. (2020) Growth hormone secretagogues: history, mechanism of action, and clinical development. JCSM Rapid Communications, Wiley 3, 25–37 3 Walker, R. F. (2006) Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin. Interv. Aging, Dove Medical Press Ltd. 1, 307–308 4 Moulin, A., Brunel, L., Verdie, P., Gavara, L., Martinez, J. and Fehrentz, J.-A. (2014) Ghrelin Receptor Ligands: Design and Synthesis of Pseudopeptides and Peptidomimetics. Curr. Chem. Biol., Bentham Science Publishers Ltd. 7, 254–270 5 &na; (2004) Pralmorelin: GHRP 2, GPA 748, growth hormone-releasing peptide 2, KP-102 D, KP-102 LN, KP-102D, KP-102LN. Drugs R. D., Springer Nature 5, 236–239 6 Furuta, S., Shimada, O., Doi, N., Ukai, K., Nakagawa, T., Watanabe, J., et al. (2004) General pharmacology of KP-102 (GHRP-2), a potent growth hormone-releasing peptide. Arzneimittelforschung, Georg Thieme Verlag KG 54, 868–880 7 Kimura, T., Shimatsu, A., Arimura, H., Mori, H., Tokitou, A., Fukudome, M., et al. (2010) Concordant and discordant adrenocorticotropin (ACTH) responses induced by growth hormone-releasing peptide-2 (GHRP-2), corticotropin-releasing hormone (CRH) and insulin-induced hypoglycemia in patients with hypothalamopituitary disorders: evidence for direct ACTH releasing activity of GHRP-2. Endocr. J., Japan Endocrine Society 57, 639–644 8 McDowell, R. S., Elias, K. A., Stanley, M. S., Burdick, D. J., Burnier, J. P., Chan, K. S., et al. (1995) Growth hormone secretagogues: characterization, efficacy, and minimal bioactive conformation. Proc. Natl. Acad. Sci. U. S. A., Proceedings of the National Academy of Sciences 92, 11165–11169 9 Camanni, F., Ghigo, E. and Arvat, E. (1998) Growth hormone-releasing peptides and their analogs. Front. Neuroendocrinol., Elsevier BV 19, 47–72 10 McGirr, R., McFarland, M. S., McTavish, J., Luyt, L. G. and Dhanvantari, S. (2011) Design and characterization of a fluorescent ghrelin analog for imaging the growth hormone secretagogue receptor 1a. Regul. Pept., Elsevier BV 172, 69–76 11 Peñalva, A., Carballo, A., Pombo, M., Casanueva, F. F. and Dieguez, C. (1993) Effect of growth hormone (GH)-releasing hormone (GHRH), atropine, pyridostigmine, or hypoglycemia on GHRP-6-induced GH secretion in man. J. Clin. Endocrinol. Metab., The Endocrine Society 76, 168–171 12 Cheng, J., Wu, T. J., Butler, B. and Cheng, K. (1997) Growth hormone releasing peptides: a comparison of the growth hormone releasing activities of GHRP-2 and GHRP-6 in rat primary pituitary cells. Life Sci., Elsevier BV 60, 1385–1392
Snapshot Sermorelin and ipamorelin are investigational peptides that stimulate endogenous growth hormone release through complementary GHRH and ghrelin receptor pathways. Preclinical and physiological data support synergistic GH pulsatility when both signaling axes are engaged, though direct combination studies remain limited. What Is Sermorelin? Sermorelin is a synthetic peptide analog of growth hormone–releasing hormone (GHRH), corresponding to the first 29 amino acids of endogenous human GHRH [1]. Sermorelin acts on the anterior pituitary and stimulates pulsatile secretion of growth hormone (GH). This preserves endogenous regulatory feedback mechanisms and the natural circadian rhythm of GH release. In research and clinical studies, sermorelin has been used as a tool to assess pituitary GH reserve and to explore age-related or functional declines in GH signaling. By activating the GHRH receptor, sermorelin promotes downstream effects on IGF-1 production, protein synthesis, and metabolic regulation [2], [3]. What Is Ipamorelin? Ipamorelin is a synthetic pentapeptide and selective growth hormone secretagogue that acts primarily through the ghrelin (GHS-R1a) receptor in the pituitary and hypothalamus [4]. Unlike other GH secretagogues, ipamorelin is designed to stimulate growth hormone release with minimal impact on other pituitary hormones, such as cortisol or prolactin. Preclinical and early human studies indicate that ipamorelin promotes physiologic, pulsatile GH secretion without significantly increasing appetite or activating broad stress pathways. Because it acts through a receptor pathway distinct from GHRH, ipamorelin is investigated for its complementary role in modulating endogenous GH signaling. Sermorelin-Ipamorelin Synergy Sermorelin and ipamorelin are often grouped together because they stimulate growth hormone release through distinct, yet convergent methods in the somatotropic axis. Sermorelin activates the GHRH receptor on pituitary somatotrophs, activating cAMP/PKA signaling to promote pulsatile GH secretion [5]. Ipamorelin, by contrast, is a ghrelin receptor (GHS-R1a) agonist, which activates complementary intracellular pathways (PLC/IP3/Ca²+-linked signaling) that also facilitate GH release [6]. Complementary Mechanisms The rationale for synergy is not simply "two peptides = more GH," but rather that GHRH and ghrelin/GHS signaling amplify each other's downstream effects at the pituitary and hypothalamic level. Experimental work shows that ghrelin and growth hormone secretagogues can potentiate GHRH-driven signaling responses in model systems expressing both receptors [7]. In addition, mechanistic studies have reported receptor-level and pathway-level cross-talk between GHRH-related signaling and ghrelin receptor biology, creating a plausible basis for amplified GH pulsatility when both pathways are engaged [8]. From a systems perspective, this pairing can be framed as: Sermorelin: provides the physiologic "go" signal via the GHRH axis. Ipamorelin: supplies a parallel "gain" signal through GHS-R1a, which can increase responsiveness of somatotrophs and increase pulse amplitude. Literature-Based Evidence Direct, peer-reviewed studies that specifically test sermorelin (GHRH 1–29) combined with ipamorelin as a named pairing are limited. However, there is evidence for class-level synergy (GHRH analogs used with ghrelin/GHS receptor agonists) showing amplified GH responses compared with either pathway alone. An in vitro study examined how GHRH and growth hormone secretagogues (GHS), like ghrelin, interact at the cellular signaling level to regulate growth hormone (GH) release [7]. A heterologous cell system expressing cloned, epitope-tagged GHRH and GHS receptors were given GHRH alone, GHS or ghrelin alone, or combined receptor activation. Effects were tracked through cAMP production and pathway-specific pharmacologic inhibition. Results showed that: GHS receptor activation alone did not affect cAMP production, whereas GHRH activation typically does. Coactivation of GHRH + GHS receptors resulted in a ~2-fold increase in cAMP compared with GHRH, and dose dependent potentiation for both GHRH and GHS. Multiple peptide GHS compounds, including GHRP-6 (similar in mechanism to ipamorelin [9]) had a combined potentiation effect. The results show a selective and receptor-specific synergy between GHRH and GHS receptors, amplifying cAMP signaling beyond what GHRH alone produces. Given this in vitro evidence, the sermorelin–ipamorelin rationale is therefore best presented as mechanistic extrapolation rather than as a conclusively proven combination therapy. Dose and Ratio From a research design standpoint, a 1:1 mass ratio (5 mg + 5 mg or 10 mg + 10 mg) can be framed as aiming to engage both upstream control systems, GHRH receptor signaling and GHS-R1a signaling, without over-weighting one pathway at the expense of the other. Beyond that general rationale, the optimal ratio has not been established in the open literature and should be treated as an empirical parameter rather than a settled standard. References 1 Walker, R. F. (2006) Sermorelin: a better approach to management of adult-onset growth hormone insufficiency? Clin. Interv. Aging, Dove Medical Press Ltd. 1, 307–308 2 Prakash, A. and Goa, K. L. (1999) Sermorelin: A review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency. BioDrugs, Springer Nature 12, 139–157 3 Khorram, O., Laughlin, G. A. and Yen, S. S. (1997) Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women. J. Clin. Endocrinol. Metab., The Endocrine Society 82, 1472–1479 4 Raun, K., Hansen, B. S., Johansen, N. L., Thøgersen, H., Madsen, K., Ankersen, M., et al. (1998) Ipamorelin, the first selective growth hormone secretagogue. Eur. J. Endocrinol. 139, 552–561 5 Aitman, T. J., Rafferty, B., Coy, D., Lynch, S. S. and Clayton, R. N. (1989) Bioactivity of growth hormone releasing hormone (1-29) analogues after SC injection in man. Peptides, Elsevier BV 10, 1–4 6 Khatib, N., Gaidhane, S., Gaidhane, A. M., Khatib, M., Simkhada, P., Gode, D., et al. (2014) Ghrelin: ghrelin as a regulatory Peptide in growth hormone secretion. J. Clin. Diagn. Res., JCDR Research and Publications 8, MC13–7 7 Cunha, S. R. and Mayo, K. E. (2002) Ghrelin and growth hormone (GH) secretagogues potentiate GH-releasing hormone (GHRH)-induced cyclic adenosine 3’,5'-monophosphate production in cells expressing transfected GHRH and GH secretagogue receptors. Endocrinology, The Endocrine Society 143, 4570–4582 8 Casanueva, F. F., Camiña, J. P., Carreira, M. C., Pazos, Y., Varga, J. L. and Schally, A. V. (2008) Growth hormone-releasing hormone as an agonist of the ghrelin receptor GHS-R1a. Proc. Natl. Acad. Sci. U. S. A., Proceedings of the National Academy of Sciences 105, 20452–20457 9 Mau, S. E., Witt, M. R., Bjerrum, O. J., Saermark, T. and Vilhardt, H. (1995) Growth hormone releasing hexapeptide (GHRP-6) activates the inositol (1,4,5)-trisphosphate/diacylglycerol pathway in rat anterior pituitary cells. J. Recept. Signal Transduct. Res., Informa UK Limited 15, 311–323
What is SS-31 peptide? SS-31 is a small, 4-amino acid, mitochondria-targeting peptide, found to have antioxidant and cell-protective effects [1]. Made up of alternating aromatic and basic amino acids, it contains a dimethyl tyrosine residue that neutralizes reactive oxygen species (ROS) and prevents lipid peroxidation [1]. Pharmacologically, SS-31 is water-soluble, stable, and resistant to enzymatic breakdown [1]. It can easily penetrate cell membranes due to its structure. It is distributed widely throughout the body, with the highest concentrations in the kidneys, and is completely excreted in urine [1]. Clinical studies show it is generally safe, with only mild side effects at the injection site, and no serious problems reported [1]. Once within cells, SS-31 rapidly accumulates in the inner mitochondrial membrane, up to 5,000 times more than in the surrounding cellular environment. Inside the mitochondria, it stabilizes cardiolipin, a critical phospholipid involved in the electron transport chain [1]. By doing so, SS-31 reduces electron leakage, preserves mitochondrial structure, and enhances ATP production [1]. Because cardiolipin damage has been implicated in various conditions such as neurodegeneration, heart failure, and mitochondrial myopathies, SS-31 has been studied as a novel therapeutic and promising candidate for conditions driven by mitochondrial dysfunction [2]. SS-31 benefits, mechanisms of action, and side effects SS-31 attaches to cardiolipin, a phospholipid found within the inner layer of the mitochondria that helps maintain structure and stability [3]. In doing so, it protects cardiolipin and supports the electron transport chain [4]. This allows SS-31 to improve ATP production and counteract the impacts of oxidative stress [4]. SS-31 also activates specific antioxidant pathways, upregulating specific proteins that help protect against oxidative stress and ferroptosis cell damage [2]. Clinical and pre clinical studies have demonstrated its protective activities in cardiac, neurological, renal, and skeletal muscle tissues [5, 6, 7, 8, 9]. In models of spinal cord injuries, it also has neuroprotective activities [10]. Mitochondrial function and apoptosis SS-31, through cardiolipin binding, preserves cristae architecture and supports efficient ATP production and electron transport [11]. As a strong antioxidant, it scavenges mitochondrial ROS to restore membrane potential and enhance the cell’s ATP generation [3]. Together, these mechanisms explain why SS-31 can maintain mitochondrial morphology, and prevent swelling and depolarization under stress conditions [12]. SS-31 upregulates SIRT1 expression, which suggests it may improve mitochondrial resilience and cellular metabolism through gene regulation [13]. Cardiolipin stabilization from SS-31 also prevents its peroxidation, reducing cytochrome C leakage and activation of apoptotic pathways [10]. SS-31 lowers caspase-3 activity, shifts specific pathways towards cell survival, and reduces DNA fragmentation to prevent apoptosis [14]. Heart health SS-31 protects and restores heart health, particularly in conditions associated with heart failure, hypertension, atherosclerosis, and decreased blood flow [15]. By binding and stabilizing within mitochondrial membranes, SS-31 lowers oxidative stress and improves energy production [16]. In models of aging hearts, it restores healthy diastolic function and lowers oxidative damage without interfering with systolic function [16]. SS-31 repairs age-related changes in important heart proteins, improving muscle relaxation and resilience [17]. In models of cardiomyopathy and heart failure, SS-31 prevents apoptosis, limits scarring and thickening of cardiac muscle, and improves overall energy efficiency [5]. This remains even when blood pressure remains high [18]. It also strengthens aerobic metabolism, helping the heart meet high energy demands [19]. Within the blood vessels, SS-31 lowers inflammation, stabilizes atherosclerotic plaques, and enhances ATP production [20]. In ischemia-reperfusion, SS-31 reduces tissue damage and speeds recovery [21]. Antioxidant and anti-inflammatory properties SS-31 can neutralize reactive oxygen species and provide protection for mitochondrial membranes [22]. By binding cardiolipin, SS-31 prevents cardiolipin peroxidation, which helps preserve mitochondrial integrity, limit cytochrome C leakage, and protect against mitochondrial dysfunction [23]. One study found SS-31 was able to prevent depletion of key antioxidant enzymes, including myeloperoxidase and superoxide dismutase, helping maintain redox balance [24]. By limiting oxidative damage, SS-31 can preserve mitochondrial energy output, limiting further ROS generation. SS-31 also has anti-inflammatory impacts, with research finding it can lower levels of TNF-α, IL-1β, and IL-6 in lung tissue. These cytokines are key mediators of inflammatory and fibrotic signaling [22]. Because high ROS amplifies profibrotic pathways, reducing ROS indirectly lowers inflammation and fibrosis. Through its impacts on myeloperoxidase, SS-31 reduces neutrophil-driven tissue injury and inflammation [22].