BPC-157 Research — Mechanism of Action, Preclinical Studies & Chemical Profile

Introduction

Body Protection Compound-157 (BPC-157) is a synthetic pentadecapeptide — a 15-amino-acid sequence — that was derived from a naturally occurring protective protein isolated from human gastric juice. First characterized by researchers at the University of Zagreb, it has been investigated across a broad range of preclinical in vitro and in vivo models over the past three decades. The compound is formally designated as a stable gastric pentadecapeptide, reflecting its resistance to proteolytic degradation in the gastrointestinal environment, a property that distinguishes it from many endogenous peptide fragments.

BPC-157 has attracted substantial interest in preclinical pharmacology because of its apparent pleiotropic activity: a single compound demonstrating reproducible effects across diverse tissue injury models, from musculoskeletal repair to gastrointestinal mucosal protection to central nervous system injury paradigms. This breadth of activity is unusual for a peptide of its size and has motivated mechanistic studies aimed at identifying the molecular pathways responsible. A 2025 systematic review published in HSS Journal (Vasireddi et al.) identified 36 qualifying preclinical studies across orthopaedic and sports medicine applications alone, underscoring the growing volume of peer-reviewed preclinical literature on this compound [1].

This article presents a structured review of BPC-157’s chemical identity, proposed mechanisms of action, and key preclinical research findings organized by organ system. It is intended to serve as a reference resource for qualified researchers evaluating BPC-157 for laboratory investigation. BPC-157 is available for research procurement at Peptide.co, where independent third-party Certificates of Analysis are provided for each lot.

Chemical Profile

BPC-157 is a well-characterized small peptide with a fully established chemical identity. The table below summarizes its key physicochemical descriptors.

Structural Considerations

The full IUPAC peptide name is glycyl-L-alpha-glutamyl-L-prolyl-L-prolyl-L-prolyl-glycyl-L-lysyl-L-prolyl-L-alanyl-L-alpha-aspartyl-L-alpha-aspartyl-L-alanyl-glycyl-L-leucyl-L-valine. The sequence contains an unusually high density of proline residues (positions 3, 4, 5, and 8), which confers structural rigidity and likely contributes to its stability against peptidase digestion. This protease resistance underpins the “stable” designation and enables the compound to persist in the gastrointestinal environment long enough to exert local mucosal effects in rodent models [2].

A 2022 pharmacokinetic study published in Frontiers in Pharmacology (He, Feng, Guo et al.) formally characterized the compound’s metabolic fate using radiolabeled tracer methods in rats and dogs, confirming rapid degradation to small peptide fragments (metabolites M1–M6) that subsequently enter normal amino acid recycling pathways [2].

Purity and Quality Reference Data

Researchers sourcing BPC-157 from Peptide.co can verify compound purity through the Peptide.co Certificate of Analysis portal. Current lot purity data are summarized below:

Full analytical documentation — including HPLC chromatograms and mass spectrometry data — is accessible via coa.peptide.co.

Mechanism of Action

Unlike classical pharmacological agents that act at a single well-defined receptor, BPC-157 is best described as a pleiotropic cytoprotective peptide — a compound that modulates multiple signaling networks simultaneously rather than engaging a single high-affinity molecular target. The mechanistic picture has been assembled incrementally across in vitro cell culture experiments and rodent in vivo studies, and the 2025 HSS Journal systematic review by Vasireddi et al. provides a current synthesis of signaling pathway evidence [1].

Angiogenic and Endothelial Signaling

The most consistently reported molecular effect of BPC-157 across multiple experimental systems is upregulation of vascular endothelial growth factor (VEGF) expression and downstream pro-angiogenic signaling. In vitro studies using human umbilical vein endothelial cells (HUVECs) have demonstrated that BPC-157 promotes endothelial cell proliferation, directed migration, and capillary tube formation — the classical hallmarks of angiogenesis [3]. At the intracellular signaling level, these effects are associated with increased phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) and downstream transcriptional activation of immediate-early response genes including c-Fos, c-Jun, and Egr-1 [1, 3].

PI3K/AKT Pro-Survival Pathway

Multiple preclinical studies have documented increased AKT phosphorylation following BPC-157 exposure. AKT (protein kinase B) is a central node in the phosphoinositide 3-kinase (PI3K) pathway that governs cell survival, anti-apoptotic programming, and metabolic regulation. Increased AKT activation is consistent with the cytoprotective phenotypes observed across tissue injury models and may partially explain the compound’s ability to attenuate ischemia-reperfusion injury in rodent organ models [1].

Growth Hormone Receptor Potentiation

A particularly informative in vitro study by Chang, Tsai, Hsu, and Pang (2014), published in Molecules, investigated BPC-157’s effects on rat Achilles tendon fibroblasts and found dose- and time-dependent increases in growth hormone receptor (GHR) expression at both the mRNA and protein levels — up to a 7-fold increase at 0.5 μg/mL over 72 hours [4]. Critically, when growth hormone (GH) was co-applied to BPC-157-pretreated fibroblasts, JAK2 phosphorylation (the primary intracellular kinase downstream of GHR activation) was significantly enhanced compared to GH alone, and cell proliferation was potentiated. This suggests that BPC-157 may prime target cells to respond more robustly to endogenous GH signaling — a sensitization mechanism rather than direct agonism [4].

Focal Adhesion Kinase and Cell Migration Programs

In vitro tendon fibroblast studies have also documented increased expression of focal adhesion kinase (FAK) and the scaffold protein paxillin following BPC-157 exposure [1]. FAK is a non-receptor tyrosine kinase that functions as a master regulator of integrin-mediated cell adhesion, spreading, and directional migration — processes that are rate-limiting steps in tissue repair and wound closure. Elevated FAK/paxillin activity is consistent with the accelerated tissue remodeling phenotypes observed in rodent injury models.

Nitric Oxide System Modulation

Nitric oxide (NO) signaling appears repeatedly in the BPC-157 preclinical literature as both a mediator and target of the compound’s activity. Unlike simple NO donors or NOS inhibitors, BPC-157 appears to modulate NO homeostasis in a context-dependent manner — upregulating endothelial NOS (Nos3) while potentially downregulating inducible NOS (Nos2) in inflammatory contexts [5]. Gene expression profiling in hippocampal ischemia-reperfusion rat models showed upregulation of both Nos3 and Nos1 alongside downregulation of Nos2 and Nfkb, suggesting a pro-vascular, anti-inflammatory rebalancing of the NO axis rather than non-specific NO elevation [5].

Anti-inflammatory Pathway Modulation

Across multiple in vitro and in vivo models, BPC-157 exposure is associated with reductions in pro-inflammatory mediators including cyclooxygenase-2 (COX-2) expression, myeloperoxidase (MPO) activity, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) [1]. These anti-inflammatory signatures are thought to be partly downstream of NF-κB suppression and partly mediated through prostaglandin system modulation. In gastric mucosal models, BPC-157 also demonstrates adaptive cytoprotection — the phenomenon whereby low-level mucosal conditioning reduces vulnerability to subsequent severe insults — consistent with engagement of cytoprotective programs including heat shock proteins HSP70 and HSP90 [6].

Preclinical Research Findings

The preclinical literature on BPC-157 spans multiple organ systems and injury paradigms. The following sections organize key findings by research domain, emphasizing peer-reviewed publications with specific experimental models and quantified outcomes.

Wound Healing and Soft Tissue Repair

Wound healing represents one of the most extensively studied domains in BPC-157 preclinical research. The comprehensive 2021 review by Seiwerth, Milavic, Vukojevic et al., published in Frontiers in Pharmacology, synthesizes findings across incisional/excisional wound models, burn injury models, diabetic ulcer models, and complex fistula models in rodents [3].

In excisional and incisional rat wound models, BPC-157 administration (via local, intraperitoneal, or oral routes) accelerated the collagen-inflammatory cell-angiogenesis triad, producing earlier granulation tissue maturation, increased mature collagen deposition, and enhanced tensile strength compared to controls. In burn injury models using mice with 20% total body surface area (TBSA) scalds, both local and systemic administration improved re-epithelialization, reduced inflammatory infiltrate, decreased tissue edema, and enhanced vascular density — with outcomes reported to exceed silver sulfadiazine controls under the study conditions [3].

Particularly noteworthy is the compound’s apparent effectiveness in diabetic wound models (alloxan-induced diabetic rats/mice), where impaired healing is a major research challenge. BPC-157 restored mature collagen organization and granulation progression in this context, with effects associated with stimulation of egr-1 and nab2 expression in intestinal epithelial cell lines [3].

A notable gene expression signature was identified using rapid wound sampling: in rodent excision skin wounds, genes including Akt1, Braf, Egfr, Egr1, Grb2, Kras, Mapk1/3/14, Nos3, Pik3cd, Plcg1, Ptk2 (FAK), Pxn (paxillin), Src, Vegfa, and others were upregulated within 2–10 minutes of BPC-157 application, implying rapid transcriptional activation of pro-repair networks [3].

Gastrointestinal Cytoprotection

BPC-157 was originally characterized in the context of gastric mucosal biology and retains one of its richest preclinical evidence bases in gastrointestinal research. The 2022 review by Sikiric, Skrtic et al. in the World Journal of Gastroenterology summarizes decades of rodent GI protection data [6].

In rat models of chemically-induced gastric and duodenal injury — including alcohol-, NSAID-, cysteamine-, and stress-induced lesions — BPC-157 demonstrated dose-dependent mucosal protection across oral, intraperitoneal, and local administration routes. The compound also healed surgically-created fistulas (colocutaneous, gastrocutaneous, esophagocutaneous, vesicovaginal, and rectovaginal) and ameliorated short bowel syndrome and inflammatory bowel disease models using TNBS- and iodoacetamide-induced colitis paradigms [6].

Mechanistically, GI cytoprotection is linked to tight junction protein regulation (ZO-1 upregulation), induction of heat shock proteins (HSP70/90), and adaptive cytoprotection phenomena. BPC-157’s resistance to gastric acid degradation (reported stable in gastric juice for >24 hours) is relevant to oral administration studies and distinguishes it from acid-labile peptides in this research context [6].

Cardiovascular and Vascular Biology

Two landmark studies in cardiovascular preclinical models merit specific attention.

Udovicic, Sever, Kavur et al. (2021) in Biomedicines investigated BPC-157 in the monocrotaline-induced rat model of pulmonary arterial hypertension (PAH) — a well-validated rodent model in which monocrotaline selectively injures pulmonary vascular endothelium, leading to progressive right ventricular failure [7]. BPC-157 administered at 10 μg/kg or 10 ng/kg (intraperitoneally or in drinking water) in either prophylactic (concurrent with monocrotaline) or therapeutic (initiated at day 14, after disease establishment) regimens produced complete elimination of the PAH phenotype: pulmonary arteriole medial hypertrophy was absent, right ventricular/left ventricular weight ratios were normalized, QT intervals and heart rate were preserved, and mortality was 0% in BPC-157 groups versus approximately 50% in controls [7].

In parallel, Sikiric et al. (2022) in the World Journal of Gastroenterology characterized BPC-157’s effects in rodent models of major vessel occlusion, including inferior vena cava ligation, Pringle maneuver (hepatic inflow occlusion), and Budd-Chiari suprahepatic obstruction [6]. In these models, BPC-157 was observed to activate collateral vascular pathways to bypass occlusions, normalize portal and caval hypertension, attenuate ischemia-reperfusion organ injury across liver, kidney, gut, and heart, and maintain platelet aggregation function and anti-thrombotic balance [6].

Central Nervous System Research

Vukojević, Milavić, Perović et al. (2021) published a dedicated CNS review in Neural Regeneration Research synthesizing the preclinical evidence for BPC-157 across neurological injury and neuropharmacological perturbation models [5].

In rat stroke models using bilateral carotid artery clamping followed by reperfusion, BPC-157 administration was associated with full resolution of spatial memory deficits (Morris water maze), locomotion abnormalities, and coordination impairments, alongside attenuated hippocampal neuronal damage. Gene expression profiling in these stroke models revealed upregulation of Egr1, Akt1, Kras, Src, Foxo, Srf, Vegfr2, Nos3, and Nos1 with concomitant downregulation of Nos2 and Nfkb — a transcriptional signature consistent with enhanced vascularization and anti-inflammatory NO rebalancing [5].

In spinal cord compression models (S2–Co1 level), BPC-157 administration countered tail paralysis, hemorrhage, necrosis, and demyelination, with functional recovery confirmed at both macroscopic and electrophysiological levels [5]. Additional CNS paradigms in which BPC-157 was investigated include: traumatic brain injury, multiple sclerosis-like (cuprizone) pathology, NSAID and paracetamol-induced encephalopathy, dopaminergic and serotonergic system perturbation models, and models of anxiety and depression-like behavior [5].

Musculoskeletal and Connective Tissue Research

The 2025 systematic review by Vasireddi, Hahamyan, Salata et al. in HSS Journal represents the highest-quality synthesis of BPC-157 musculoskeletal preclinical data to date [1]. Across 35 qualifying preclinical studies, the authors identified consistent evidence for:

• Muscle repair: Improved functional and histological outcomes in muscle transection and crush injury models, with reduced inflammatory infiltrate and accelerated fiber regeneration.
• Tendon healing: Faster biomechanical strength recovery in Achilles and quadriceps tendon transection models, with increased vascularity and VEGF expression at repair sites.
• Ligament repair: Structural and functional improvement in medial collateral ligament (MCL) transection models.
• Bone regeneration: Accelerated healing in fracture non-union models and critical-size bone defect paradigms.

The mechanistic underpinning for musculoskeletal effects was clarified by the in vitro work of Chang et al. (2014) in rat tendon fibroblasts, which demonstrated that BPC-157 sensitizes these cells to GH signaling via GHR upregulation and potentiated JAK2 phosphorylation — a plausible mechanism for the observed pro-repair tissue effects in tendon and connective tissue models [4].

Ocular Research

An emerging research domain is BPC-157’s investigation in ocular models. Sikiric, Kokot, Kralj et al. (2023) published a dedicated preclinical review in Pharmaceuticals covering glaucoma, corneal injury, dry eye, and retinal ischemia paradigms [8]. In rat models of elevated intraocular pressure (IOP) produced by episcleral vein cauterization, topical, oral, and intraperitoneal BPC-157 rapidly normalized IOP and preserved retinal ganglion cells and optic nerve architecture [8]. In corneal injury models including perforating incisions and total epithelial debridement, BPC-157 accelerated healing while preventing neovascularization and maintaining corneal transparency [8].

Storage & Handling for Research Use

Proper storage and handling are essential to maintaining the chemical integrity of BPC-157 and ensuring data reproducibility in preclinical experiments. The following guidelines are based on standard peptide chemistry best practices applicable to research-grade lyophilized peptides.

Lyophilized (Dry Powder) Form

• Long-term storage: −20°C to −80°C in a sealed, desiccated container, protected from light and moisture. Under these conditions, lyophilized BPC-157 is expected to retain integrity for extended periods (typically 24+ months when properly sealed).
• Short-term (working stock): −20°C is sufficient for periods up to several months if the vial is tightly resealed after each access and moisture exposure is minimized.
• Warm-up protocol: Allow sealed vials to equilibrate to room temperature prior to opening to prevent condensation on the lyophilized cake, which accelerates degradation.
• Humidity control: Open vials only under dry, inert conditions where possible. Peptides are hygroscopic and will absorb atmospheric moisture rapidly upon exposure.

Reconstituted Solutions

• Reconstitution solvent: For research applications, BPC-157 is typically reconstituted in sterile, bacteriostatic water, 0.9% NaCl, or 0.5–1% acetic acid (for improved initial solubility). Solvent selection should align with the experimental administration route and downstream assay requirements.
• Aliquoting: After reconstitution, divide into single-use aliquots to avoid repeated freeze-thaw cycles, which promote aggregation and peptide bond hydrolysis.
• Refrigerated use: Reconstituted solutions may be used within approximately 7 days when stored at 2–8°C in sealed vials; for longer storage, frozen aliquots at −20°C are preferred.
• Avoid: Repeated freeze-thaw cycling, exposure to direct light, elevated pH (alkaline conditions), and metal ion contamination, all of which may accelerate oxidation or aggregation.

For calculating stock concentrations and preparing dilutions, researchers may use the Peptide.co Reconstitution Calculator, which automates volume and concentration conversions for common research applications.

Safety Profile

The preclinical safety database for BPC-157 is relatively extensive for a research peptide and encompasses multiple species, routes of administration, and toxicological endpoints. The following summary is based on the published animal safety literature; human safety data do not exist in the context of approved clinical studies.

Formal Preclinical Toxicology Package

The most comprehensive single toxicology assessment was published by Xu, Sun, Ren et al. (2020) in Regulatory Toxicology and Pharmacology (PMID: 32334036) [9]. This study conducted a formal GLP-aligned toxicology program in four species (mice, rats, rabbits, and dogs) and reported the following:

• Single-dose toxicity: No test-article-related adverse effects at any dose level tested; a lethal dose in 50% of animals (LD₅₀) was not achieved in any species.
• Repeat-dose toxicity: Well tolerated across all species. In dogs at 2 mg/kg, a reversible decrease in serum creatinine was noted and attributed to pharmacological activity (resolved fully after a two-week recovery period); no other organ-specific toxicity signals were observed.
• Local tolerance: Mild, transient local irritation at injection sites; no necrosis or systemic inflammatory responses.
• Genetic toxicity: Negative in standard mutagenicity and genotoxicity assays.
• Embryo-fetal development: No evidence of developmental toxicity or teratogenicity in the tested species and dose ranges.

Systematic Review Safety Summary

The 2025 Vasireddi et al. systematic review in HSS Journal synthesized safety data across multiple independent preclinical studies and found no reports of acute toxicity, hepatotoxicity, nephrotoxicity, or histological organ pathology in rodents receiving BPC-157 at doses ranging from 6 μg/kg to 20 mg/kg (intramuscular, intraperitoneal, intravenous, or oral) over durations up to six weeks [1].

Limitations of the Safety Dataset

The available safety data have important scope limitations that researchers should consider:

• Most studies are short in duration (≤6 weeks); long-term chronic exposure and carcinogenicity studies are not established in the peer-reviewed literature reviewed here.
• No randomized controlled human safety trials exist. Extrapolation of animal safety data to humans is not scientifically valid without clinical validation.
• Route-of-administration-specific safety profiles may differ; the majority of formal toxicology data are from parenteral (IP, IV, IM) and oral routes in rodents.

BPC-157 is supplied by Peptide.co for preclinical research use only. Researchers are responsible for implementing appropriate institutional biosafety protocols and ethical oversight for all animal studies.

BPC-157 vs Related Compounds

Researchers studying tissue repair and cytoprotection often evaluate BPC-157 alongside other peptides and growth factors with overlapping research applications. Understanding the distinctions between these compounds at the mechanistic and experimental level is critical for experimental design and data interpretation.

BPC-157 vs TB-500 (Thymosin Beta-4)

TB-500 (a synthetic analog of thymosin beta-4) is a 43-amino-acid peptide originally characterized for its role in actin dynamics and cytoskeletal organization. It is frequently investigated in musculoskeletal and cardiovascular repair contexts. The two compounds are among the most commonly compared repair-associated peptides in preclinical research, but they differ substantially in their primary molecular targets and proposed mechanisms:

It should be emphasized that the two compounds are mechanistically distinct and are not interchangeable in research design. Selection between them should be driven by the specific biological question, target tissue, and experimental model under investigation.

BPC-157 vs Classical Growth Factors (VEGF, PDGF, EGF)

BPC-157 is frequently described as modulating growth factor signaling pathways rather than acting as a growth factor itself. Unlike recombinant VEGF, PDGF-BB, or EGF — which are direct ligands for cognate receptor tyrosine kinases — BPC-157 appears to function upstream or in parallel with these pathways, upregulating the expression and activity of their downstream signaling components [1]. This indirect mode of action has practical implications for preclinical researchers: BPC-157 may amplify endogenous growth factor responses rather than substituting for them.

BPC-157 vs Single-Target NO Modulators

Unlike selective NOS inhibitors (e.g., L-NAME) or simple NO donors, BPC-157 modulates the nitric oxide system in a context-sensitive, multi-isoform manner — upregulating eNOS while attenuating inflammatory iNOS expression. This nuanced NO modulation may account for some of the compound’s vascular protective effects without the non-selective hemodynamic consequences associated with global NOS inhibition or systemic NO supplementation [5, 6].

Frequently Asked Questions

References

1. Vasireddi N, Hahamyan H, Salata MJ, Karns M, Calcei JG, Voos JE, Apostolakos JM. Emerging Use of BPC-157 in Orthopaedic Sports Medicine: A Systematic Review. HSS J. 2025 (Online ahead of print). PMC: PMC12313605.
2. He L, Feng D, Guo H, Zhou Y, Li Z, Zhang K, Zhang W, Wang S, Wang Z, Hao Q, Zhang C, Gao Y, Gu J, Zhang Y, Li W, Li M. Pharmacokinetics, distribution, metabolism, and excretion of body-protective compound 157, a potential drug for treating various wounds, in rats and dogs. Front Pharmacol. 2022;13:1026182. DOI: 10.3389/fphar.2022.1026182. PMC: PMC9794587.
3. Seiwerth S, Milavic M, Vukojevic J, Gojkovic S, Krezic I, Batelja Vuletic L, Horvat Pavlov K, Petrovic A, Sikiric S, Vranes H, Prtoric A, Zizek H, Durasin T, Dobric I, Staresinic M, Strbe S, Knezevic M, Sola M, Kokot A, Sever M, Lovric E, Skrtic A, Boban Blagaic A, Sikiric P. Stable Gastric Pentadecapeptide BPC 157 and Wound Healing. Front Pharmacol. 2021;12:627533. DOI: 10.3389/fphar.2021.627533. PMC: PMC8275860.
4. Chang CH, Tsai WC, Hsu YH, Pang JH. Pentadecapeptide BPC 157 Enhances the Growth Hormone Receptor Expression in Tendon Fibroblasts. Molecules. 2014;19(12):19172–19180. DOI: 10.3390/molecules191219151. PMC: PMC6271067.
5. Vukojević J, Milavić M, Perović D, Ilić S, Zemba Čilić A, Đuran N, Štrbe S, Zoričić Z, Filipčić I, Brečić P, Seiverth S, Sikirić P. Pentadecapeptide BPC 157 and the central nervous system. Neural Regen Res. 2022;17(3):482–487. DOI: 10.4103/1673-5374.320969. PMC: PMC8504390.
6. Sikiric P, Skrtic A, Gojkovic S, Krezic I, Zizek H, Lovric E, Sikiric S, Knezevic M, Strbe S, Milavic M, Kokot A, Boban Blagaic A, Seiwerth S. Cytoprotective gastric pentadecapeptide BPC 157 resolves major vessel occlusion disturbances, ischemia-reperfusion injury following Pringle maneuver, and Budd-Chiari syndrome. World J Gastroenterol. 2022;28(1):23–46. DOI: 10.3748/wjg.v28.i1.23. PMC: PMC8793015.
7. Udovicic M, Sever M, Kavur L, Loncaric K, Barisic I, Balenovic D, Zivanovic Posilovic G, Strinic D, Uzun S, Batelja Vuletic L, Sikiric S, Skrtic A, Drmic D, Boban Blagaic A, Lovric Bencic M, Seiwerth S, Sikiric P. Stable Gastric Pentadecapeptide BPC 157 Therapy for Monocrotaline-Induced Pulmonary Hypertension in Rats Leads to Prevention and Reversal. Biomedicines. 2021;9(7):822. DOI: 10.3390/biomedicines9070822. PMC: PMC8301325.
8. Sikiric P, Kokot A, Kralj T, Zlatar M, Masnec S, Lazic R, Loncaric K, Oroz K, Sablic M, Boljesic M, Antunovic M, Sikiric S, Strbe S, Stambolija V, Beketic Oreskovic L, Kavelj I, Novosel L, Zubcic S, Krezic I, Skrtic A, Jurjevic I, Boban Blagaic A, Seiwerth S, Staresinic M. Stable Gastric Pentadecapeptide BPC 157—Possible Novel Therapy of Glaucoma and Other Ocular Conditions. Pharmaceuticals (Basel). 2023;16(8):1065. DOI: 10.3390/ph16081065. PMC: PMC10385428.
9. Xu C, Sun L, Ren F, Huang P, Tian Z, Cui J, Zhang W, Wang S, Zhang K, He L, Zhang W, Zhang C, Hao Q, Zhang Y, Li M, Li W. Preclinical safety evaluation of body protective compound-157, a potential drug for treating various wounds. Regul Toxicol Pharmacol. 2020;114:104665. DOI: 10.1016/j.yrtph.2020.104665. PMID: 32334036.
10. PubChem. BPC-157. National Center for Biotechnology Information. CID 9941957. Available at: https://pubchem.ncbi.nlm.nih.gov/compound/9941957.