{"product_id":"pancragen-peptide-pancreas-longevity-research","title":"Pancragen Peptide - Pancreas Longevity Research","description":"\u003ch3\u003e\u003cstrong\u003ePancragen Description\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003ePancragen is a small molecule made of four amino acids that targets the pancreas to help it work better.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThe pancreas is an organ that makes insulin to control blood sugar and enzymes to digest food. Over time or with diseases like diabetes, the cells in the pancreas can become less effective at their jobs.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003ePancragen enters pancreatic cells and interacts with their DNA to turn on genes needed for healthy cell development. This process helps both the cells that produce insulin and those that make digestive enzymes to mature and function properly.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eResearch in lab cells and animals shows it can support better blood sugar regulation by improving pancreatic performance. It also appears to protect cells from stress and encourage renewal in older or damaged pancreatic tissue.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIn studies with older people who have type 2 diabetes, it helped improve how their bodies handled sugar.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eScientists see potential uses for supporting metabolic health and addressing pancreas-related issues in aging.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003ePancragen offers a way to support the pancreas at a deep cellular level rather than just managing symptoms.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eMolecular Mechanisms of Action\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003ePancragen, also referred to as the tetrapeptide KEDW with the amino acid sequence Lys-Glu-Asp-Trp, functions as an organ-specific bioregulator peptide that selectively targets pancreatic tissue to restore and maintain cellular activity at the molecular level.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eAs a specialist in peptide synthesis and biochemistry, you will appreciate its design as a short-chain synthetic analog modeled after naturally occurring regulatory peptides isolated from pancreatic extracts, enabling precise modulation of gene expression without broad systemic disruption.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThe pancreas comprises two primary functional compartments:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ethe exocrine portion dominated by acinar cells that synthesize and secrete digestive enzymes such as amylase, lipase, and proteases,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand the endocrine islets of Langerhans containing beta cells responsible for insulin production and secretion, alpha cells that release glucagon, and other cell types including delta and PP cells that fine-tune metabolic signaling.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eIn physiological states, these compartments maintain tight coordination through transcription factor networks that govern cell identity, proliferation, differentiation, and survival.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eHowever, aging, chronic metabolic stress, or inflammatory conditions lead to progressive decline characterized by:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ereduced expression of key differentiation markers,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eincreased apoptosis,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ededifferentiation of beta cells,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eexcess alpha cell activity contributing to hyperglucagonemia,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand impaired acinar cell function manifesting as reduced enzyme output or fibrosis.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003ePancragen addresses these disruptions directly through its ability to penetrate cellular and nuclear membranes owing to its low molecular weight of approximately 576 Da and amphiphilic properties, allowing it to reach chromatin structures and exert epigenetic control over gene transcription.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eEpigenetic Regulation and Transcription Factor Modulation\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003eAt the molecular level, Pancragen’s mechanism of action centers on its direct interaction with DNA and associated chromatin complexes, including histone proteins, which facilitates targeted modulation of promoter regions and chromatin accessibility.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThis interaction occurs via binding to specific DNA motifs, such as ACCT sequences commonly found in regulatory elements of pancreas-specific genes, enabling the peptide to influence nucleosome positioning and histone modifications without altering the underlying DNA sequence.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThe result is an epigenetic reprogramming that shifts transcriptional profiles toward those observed in younger, healthier pancreatic cells.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eCentral to this process is the upregulation of master transcription factors essential for pancreatic cell lineage commitment and maturation.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThese include:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ePDX1 (pancreatic and duodenal homeobox 1),\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ePTF1A (pancreas transcription factor 1a),\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ePAX6,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eFOXA2,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eNKX2.2,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand PAX4.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003ePDX1 acts as a foundational regulator that orchestrates both exocrine and endocrine development by binding to insulin gene promoters and coordinating beta cell identity, glucose sensing, and insulin biosynthesis.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIts diminished expression in aging or diabetic states contributes to beta cell dysfunction and glucose intolerance.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003ePancragen enhances PDX1 levels in both acinar and islet contexts, thereby restoring insulin gene transcription and supporting beta cell resilience against metabolic overload.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eSimilarly, PTF1A drives acinar cell differentiation by forming complexes that activate digestive enzyme gene clusters, promoting exocrine tissue integrity and enzyme secretion capacity often compromised in chronic pancreatitis or age-related atrophy.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIn endocrine lineages, upregulation of PAX6 facilitates beta cell maturation and insulin granule formation, while FOXA2 serves as a pioneer factor that opens chromatin for downstream endocrine gene activation and maintains islet architecture.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eNKX2.2 and PAX4 further refine beta cell specification by repressing alpha cell programs and promoting insulin-positive cell survival, countering the alpha-to-beta imbalance seen in type 2 diabetes where excess glucagon exacerbates hyperglycemia.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThese transcription factors operate in a hierarchical network, with Pancragen amplifying their coordinated expression to drive de novo differentiation and functional maturation of progenitor-like states within existing pancreatic tissue.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eCellular Repair and Anti-Apoptotic Signaling\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003eBeyond transcription factor induction, Pancragen exerts broader epigenetic effects by modulating DNA methylation patterns at key promoters such as those of:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ePDX1,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eNGN3,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand PAX6.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eThis effectively reverses age-associated hypermethylation that silences these loci and restores youthful accessibility for RNA polymerase II recruitment.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThis leads to downstream increases in functional effector molecules, including matrix metalloproteinases MMP2 and MMP9, which facilitate extracellular matrix remodeling essential for tissue repair, cell migration, and vascular integrity within the pancreatic microenvironment.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eSerotonin levels rise as well, supporting paracrine signaling that enhances beta cell proliferation and insulin release while modulating inflammation.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eProliferation markers such as PCNA and Ki-67 are elevated, indicating enhanced cell cycle entry in quiescent or senescent populations.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eAt the same time, pro-apoptotic proteins like:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ep53,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ecaspase-3,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand cathepsin B\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eare suppressed in favor of anti-apoptotic Mcl-1, thereby tipping the balance toward cell survival and mass preservation.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThese molecular cascades collectively mitigate oxidative stress and low-grade inflammation by normalizing cytokine profiles, including reductions in TNF-α, and improving endothelial function in pancreatic vasculature.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThe net outcome is a regenerative-like state where pancreatic cells regain competence in:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eglucose-stimulated insulin secretion,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eglucagon suppression,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand enzymatic output.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eThis directly translates to improved systemic carbohydrate metabolism and reduced insulin resistance through better beta cell responsiveness and peripheral tissue sensitization.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003ePotential Research Applications\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003ePotential research applications stem logically from this molecular restoration of pancreatic homeostasis.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIn type 2 diabetes, where beta cell dedifferentiation and apoptosis drive progressive insulin deficiency amid peripheral resistance, Pancragen’s ability to reactivate PDX1 and related networks offers a pathway to enhance endogenous insulin production and normalize alpha-beta cell ratios.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eFor age-related metabolic decline, common in geriatric populations with impaired glucose tolerance, the peptide’s rejuvenating effects on gene expression profiles could support preventive maintenance of pancreatic endocrine function, mitigating the decline in beta cell mass and secretory capacity that accompanies senescence.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIn chronic pancreatitis, characterized by:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eacinar cell loss,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003efibrosis,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand exocrine insufficiency,\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eupregulation of PTF1A and MMPs may promote tissue remodeling and enzyme-producing cell recovery, supporting digestive and endocrine resilience.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eBroader metabolic syndrome contexts benefit from its endothelioprotective actions, which preserve microvascular health and reduce vascular complications linked to chronic hyperglycemia.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eAs a bioregulator, Pancragen aligns with targeted peptide research by exploiting short-sequence specificity to avoid off-target effects, making it suitable for integration into protocols focused on regenerative endocrinology or geroprotection where conventional approaches fall short in addressing cellular senescence.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eAnimal Research Findings\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003eSummaries of animal trials highlight consistent mechanistic validation across models.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIn vitro studies utilizing primary cultures of pancreatic acinar and islet cells from embryonic, young adult, and aged sources demonstrate that Pancragen treatment restores differentiation factor expression.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThis effect is particularly pronounced in aged cultures where baseline levels of:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ePDX1,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ePTF1A,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ePAX6,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eFOXA2,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eNKX2.2,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand PAX4\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eare diminished.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eThis leads to:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eincreased maturation markers,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eelevated MMP2\/9 and serotonin,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eheightened proliferation indices (PCNA and Ki-67),\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand reduced apoptotic signaling.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eIn rodent models of experimental diabetes induced by streptozotocin, Pancragen administration normalizes blood glucose homeostasis through enhanced beta cell insulin output and suppressed excess glucagon.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eMorphological improvements include:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ereduced beta cell apoptosis,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003erestored proliferative balance,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand improved islet architecture.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eAdditionally, mesenteric capillary endothelial function is preserved with decreased adhesion and improved permeability, underscoring its protective role against diabetic vasculopathy in the pancreatic bed.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003ePrimate studies in aged rhesus monkeys provide translational insight, revealing:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eenhanced glucose disappearance rates,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eimproved glucose utilization following glucose challenges,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand normalized plasma insulin and C-peptide dynamics.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eThese endocrine corrections persist for weeks post-intervention, consistent with the epigenetic nature of its gene regulatory actions.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eHuman Research and Metabolic Effects\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003eHuman trial summaries, though derived from focused cohorts, reinforce these preclinical observations in real-world metabolic contexts.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eInvestigations involving elderly participants with type 2 diabetes mellitus, often comorbid with impaired glucose tolerance or pancreatitis, report:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003ereductions in fasting glucose concentrations,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eimproved oral glucose tolerance responses,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003edecreased circulating insulin levels,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand lowered insulin resistance indices such as HOMA-IR.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eThese glycemic and sensitivity improvements align directly with Pancragen’s molecular upregulation of beta cell differentiation factors and anti-apoptotic pathways.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eClinical observations further note benefits in mixed cohorts experiencing:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eage-related metabolic disturbances,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003epancreatic inflammation,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand impaired endocrine function.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eAcross these datasets, Pancragen emerges as well tolerated while supporting pancreatic cellular functional activity and broader metabolic stabilization.\u003c\/span\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cstrong\u003eSummary\u003c\/strong\u003e\u003c\/h3\u003e\n\u003cp\u003e\u003cspan\u003eIn synthesis, Pancragen exemplifies how short peptide bioregulators can interface with nuclear machinery to orchestrate comprehensive pancreatic cell reprogramming.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eIts actions at the level of:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003etranscription factor networks,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eepigenetic regulation,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eanti-apoptotic signaling,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eextracellular matrix remodeling,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand endocrine restoration\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eprovide a foundation for regenerative peptide strategies that prioritize cellular rejuvenation over symptomatic palliation.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eAnimal and human evidence consistently converge on:\u003c\/span\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\u003cspan\u003eenhanced glucose homeostasis,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eimproved tissue integrity,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003ebetter insulin signaling,\u003c\/span\u003e\u003c\/li\u003e\n\u003cli\u003e\u003cspan\u003eand restoration of pancreatic cellular function.\u003c\/span\u003e\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cspan\u003eThis positions Pancragen as a compelling candidate for advanced peptide research applications in endocrinology, metabolic biology, and gerontology.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan style=\"font-kerning: none;\"\u003eDiscover how pancreatic bioregulator peptides are researched for digestive tissue homeostasis and metabolic signaling.\u003c\/span\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan style=\"font-kerning: none;\"\u003e→ \u003ca href=\"https:\/\/www.peptideregenesis.com\/blogs\/peptide-blog\/what-are-bioregulators\"\u003e\u003cspan\u003eWhat Are Bioregulator Peptides?\u003c\/span\u003e\u003c\/a\u003e\u003c\/span\u003e\u003c\/strong\u003e\u003c\/p\u003e","brand":"PRG","offers":[{"title":"Capsules","offer_id":53090083733770,"sku":null,"price":140.0,"currency_code":"EUR","in_stock":true},{"title":"Vial","offer_id":53090083766538,"sku":null,"price":0.0,"currency_code":"EUR","in_stock":false},{"title":"Pre-filled Pen","offer_id":53090083799306,"sku":null,"price":0.0,"currency_code":"EUR","in_stock":false}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0908\/7113\/6522\/files\/PANCRAGEN1.png?v=1779457750","url":"https:\/\/www.peptideregenesis.com\/products\/pancragen-peptide-pancreas-longevity-research","provider":"PRG","version":"1.0","type":"link"}