{"product_id":"retatrutid-40mg","title":"Retatrutide 40mg","description":"\u003cp\u003e\u003cspan\u003eRetatrutid is a peptide acting as a triple receptor agonist for GLP-1 receptors (GLP-1R), GIP receptors (GIPR), and glucagon receptors (GCGR). It enhances insulin secretion by activating GLP-1R, inhibits glucagon release, delays gastric emptying, and increases satiety; activates GIPR to enhance insulin sensitivity and regulate lipid metabolism; activates GCGR to promote energy expenditure, inhibit hepatic gluconeogenesis, and reduce hepatic fat deposition. This multi-target synergistic action makes it superior to traditional single-target GLP-1 drugs in lowering blood glucose, reducing body weight, and improving hepatic fat deposition.\u003c\/span\u003e\u003c\/p\u003e\u003cdiv\u003e \u003c\/div\u003e\u003cdiv\u003eThe peptide will be provided as lyophilized powder to ensure maximum stability.\u003c\/div\u003e\u003cdiv\u003e\u003c\/div\u003e\u003cdiv\u003e\u003cstrong\u003eWhat is Retatrutid?\u003c\/strong\u003e\u003c\/div\u003e\u003cdiv\u003e\u003cstrong\u003e\u003c\/strong\u003e\u003c\/div\u003e\u003cdiv\u003eRetatrutid is a peptide drug acting as a triple agonist of the glucose-dependent insulinotropic polypeptide receptor (GIPR), glucagon-like peptide-1 receptor (GLP-1R), and glucagon receptor (GCGR), targeting conditions such as obesity and type 2 diabetes.\u003c\/div\u003e\u003cdiv\u003e\u003cstrong\u003e\u003cspan\u003eRetatrutid Structure\u003c\/span\u003e\u003c\/strong\u003e\u003c\/div\u003e\u003cdiv\u003e\n\u003cstrong\u003e\u003cspan\u003e\u003cimg alt=\"\" src=\"https:\/\/cdn.shopify.com\/s\/files\/1\/0813\/1759\/3312\/files\/993024f9-25ff-4e7a-b6b3-e5e1411fd322.png?v=1782900264\"\u003e\u003c\/span\u003e\u003c\/strong\u003e\u003cp\u003eSequence: YA⊃1;QGTFTSDYSI-L⊃2;LDKK⁴AQA⊃1;AFIEYLLEGGPSSGAPPPS⊃3;\u003c\/p\u003e\n\u003cp\u003eMolecular Formula: C\u003csub\u003e221\u003c\/sub\u003eH\u003csub\u003e342\u003c\/sub\u003eN\u003csub\u003e46\u003c\/sub\u003eO\u003csub\u003e68\u003c\/sub\u003e\u003c\/p\u003e\n\u003cp\u003eMolecular Weight: 4731 g\/mol\u003c\/p\u003e\n\u003cp\u003eCAS Number: 2381089-83-2\u003c\/p\u003e\n\u003cp\u003ePubChem CID: 171390338\u003c\/p\u003e\n\u003cp\u003eSynonyms：LY3437943\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eRetatrutid Research\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eWhat is the research background for Retatrutid?\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eThe global prevalence of obesity and type 2 diabetes continues to rise, posing a significant public health challenge. Existing single- or dual-target drugs have limitations in efficacy and safety. Based on the theory of multi-target synergistic regulation via the gastrointestinal insulin axis, research has revealed complementary roles of GLP-1, GIP, and glucagon in metabolic regulation, providing a theoretical foundation for developing multi-receptor agonists.\u003c\/p\u003e\n\u003cp\u003eBuilding on prior dual-target drug development experience, researchers designed and optimized Retatrutid based on the structural characteristics and signaling mechanisms of these triple receptors. By simultaneously activating GLP-1R, GIPR, and GCGR, it achieves more potent glycemic control and weight reduction.\u003c\/p\u003e\n\u003cp\u003eWhat is the mechanism of action for Retatrutid?\u003c\/p\u003e\n\u003cp\u003eReceptor Agonism\u003c\/p\u003e\n\u003cp\u003eRetatrutid functions as a triple receptor agonist targeting GLP-1, GCGR, and GIP receptors\u003csup\u003e[1]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eGLP-1 receptor agonism: GLP-1 is an incretin hormone secreted by intestinal L cells. Upon binding to GLP-1 receptors, Retatrutid promotes insulin secretion in a glucose-concentration-dependent manner. During hyperglycemia, Retatrutid binds to GLP-1 receptors, activating downstream signaling pathways that prompt pancreatic β-cells to secrete insulin and lower blood glucose levels. It also inhibits glucagon secretion and reduces hepatic glucose output, further stabilizing blood glucose. GLP-1 receptor agonism also delays gastric emptying, increases satiety, and reduces food intake, aiding in weight management\u003csup\u003e[2]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eGCGR receptor agonism: Glucagon typically acts during hypoglycemia to elevate blood glucose levels. Retatrutid's agonist action on GCGR is complex. In adipose tissue, it promotes lipolysis and increases fatty acid oxidation, thereby enhancing energy expenditure. In the liver, moderate GCGR agonism may regulate processes like gluconeogenesis, optimizing hepatic metabolic function. This prevents excessive gluconeogenesis from causing hyperglycemia while maintaining sufficient blood glucose stability to meet the body's energy demands\u003csup\u003e[1]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eGIP receptor agonism: GIP, another incretin hormone, is secreted by K cells in the duodenum and jejunum after meals. Retatrutid's GIP receptor agonism enhances insulin secretion, synergizing with GLP-1 to improve glucose regulation. Conversely, GIP receptor activation may influence lipid metabolism and energy balance. Brzozowska P's research indicates that GIP promotes glucose uptake and lipid synthesis in adipocytes. However, under Retatrutid's influence, GIP signaling is modulated to optimize energy utilization rather than solely promoting fat storage, thereby aiding weight management\u003csup\u003e[1]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003e\u003cimg alt=\"\" src=\"https:\/\/cdn.shopify.com\/s\/files\/1\/0813\/1759\/3312\/files\/6a353479-4a12-4275-9cbe-51dfc761a962.png?v=1782900730\"\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cspan\u003eFigure 1 Retatrutid’s mechanisms of action\u003c\/span\u003e\u003csup\u003e[3]\u003c\/sup\u003e\u003cspan\u003e.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003eComprehensive Regulation of Metabolic Processes\u003c\/p\u003e\n\u003cp\u003eEnergy Metabolism Regulation: By activating the three receptors mentioned above, Retatrutid comprehensively regulates energy metabolism. It promotes lipolysis, increasing fatty acid entry into mitochondria for β-oxidation and enhancing energy expenditure. It reduces lipogenesis by inhibiting fatty acid uptake and triglyceride synthesis in adipocytes, thereby altering the body's energy storage and expenditure balance to facilitate weight loss. In relevant animal studies and clinical trials by Jastreboff A M, Retatrutid administration increased energy expenditure rates and progressively reduced body fat content in obese subjects\u003csup\u003e[4]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eGlucose Metabolism Regulation: Retatrutid modulates blood glucose through multiple pathways. Beyond stimulating insulin secretion via GLP-1 and GIP receptor activation, it influences hepatic glucose metabolism by regulating GCGR. It suppresses excessive hepatic gluconeogenesis, reduces glucose output, and simultaneously enhances peripheral tissue glucose uptake and utilization, thereby maintaining normal blood glucose levels. This is particularly crucial for obese patients with type 2 diabetes, effectively controlling blood glucose and improving diabetic conditions\u003csup\u003e[2]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eLiver Metabolic Regulation: Within the liver, Retatrutid not only modulates glucose metabolism but also influences lipid metabolism. It reduces hepatic triglyceride synthesis and accumulation, improves hepatic steatosis, and holds potential therapeutic value for non-alcoholic fatty liver disease (NAFLD). In clinical trials involving participants with metabolic dysfunction-associated fatty liver disease (MDAFLD), Retatrutid significantly reduced hepatic fat content, demonstrating its positive regulatory effect on hepatic metabolism\u003csup\u003e[5]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003e Effects on Gastrointestinal Function\u003c\/p\u003e\n\u003cp\u003eRetatrutid delays gastric emptying by activating GLP-1 receptors. Slower gastric emptying prolongs food residence time in the stomach, generating sustained satiety and reducing subsequent food intake. Simultaneously, it may influence gut hormone secretion and intestinal motility, further regulating gastrointestinal digestion and nutrient absorption processes, thereby comprehensively affecting energy intake and body weight\u003csup\u003e\u003cspan\u003e \u003c\/span\u003e[2]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003e \u003c\/p\u003e\n\u003cp\u003eWhat is the synergistic mechanism between Retatrutid's agonistic effects on GLP-1, GCGR, and GIP receptors?\u003c\/p\u003e\n\u003cp\u003eSynergy in Energy Metabolism Regulation\u003c\/p\u003e\n\u003cp\u003eIncreased Energy Expenditure: Activation of GCGR promotes glycogenolysis and gluconeogenesis to elevate blood glucose levels. It also enhances energy expenditure by increasing lipid metabolism and suppressing food intake through central satiety. GLP-1R agonists stimulate insulin secretion and exert cardioprotective and neuroprotective effects, while also reducing energy intake by delaying gastric emptying and suppressing appetite. While GIPR activation in adipose tissue promotes lipid accumulation, its central activation reduces food intake and alleviates weight gain. Retatrutid simultaneously targets these three receptors, establishing a new equilibrium between energy intake and expenditure. This more effectively achieves an energy deficit, thereby facilitating weight loss.\u003c\/p\u003e\n\u003cp\u003eRegulating lipid metabolism: GCGR agonism enhances lipid metabolism, while GIPR activation in adipose tissue also influences lipid metabolism. GLP-1R agonists may indirectly affect lipid metabolism through mechanisms such as improving insulin sensitivity. Their synergistic action better regulates fat synthesis, breakdown, and transport, reducing fat accumulation and improving body fat distribution. For instance, studies in obese patients showed that after using Retatrutid for a period, body fat percentage decreased and lipid profiles improved to some extent, suggesting its synergistic effects in regulating fat metabolism\u003csup\u003e[6]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eSynergistic Effects in Glucose Regulation\u003c\/p\u003e\n\u003cp\u003eEnhanced Insulin Secretion: GLP-1R agonists lower blood glucose by binding to GLP-1 receptors and promoting insulin secretion. GIP similarly stimulates pancreatic β-cells to produce insulin secretion effects similar to those induced by dietary intake. Retatrutid, which simultaneously activates GLP-1R and GIPR, significantly enhances insulin secretion, thereby more effectively lowering blood glucose levels. Although GCGR is typically associated with elevated blood glucose, its effects—such as promoting energy expenditure—can indirectly contribute to glucose stability when synergistically acting with receptors like GLP-1R. Furthermore, the combined use of GLP-1 and GCGR selectively counteracts the hyperglycemic risk induced by GCGR, enabling more precise and effective glucose regulation.\u003c\/p\u003e\n\u003cp\u003eRegulating Glucose Homeostasis: The synergistic activation of these three receptors extends beyond mere insulin secretion to encompass comprehensive glucose homeostasis regulation. By influencing glucose uptake, utilization, and storage across multiple tissues including liver, muscle, and adipose, Retatrutid maintains blood glucose within a relatively stable range, preventing significant fluctuations. In a study by Nicholls S involving type 2 diabetes patients, Retatrutid administration resulted in a significant reduction in glycated hemoglobin levels, indicating its positive impact on long-term glycemic control and demonstrating the synergistic effects of the three receptors in regulating glucose homeostasis\u003csup\u003e\u003cspan\u003e \u003c\/span\u003e[6]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eSynergistic Activation of Signal Transduction Pathways\u003c\/p\u003e\n\u003cp\u003eCommon Signal Pathway Activation: GLP-1R, GCGR, and GIPR primarily signal through G (Gαs) proteins. When Retatrutid acts on these three receptors, it converges to activate shared downstream pathways such as the cAMP-PKA pathway. This shared pathway activation enhances signal transduction efficiency and potency, amplifying regulatory effects on cellular metabolism and physiological functions.\u003c\/p\u003e\n\u003cp\u003eCoordinating distinct pathways: While sharing common pathways, each receptor also activates unique signaling networks. Retatrutid modulates these distinct pathways synergistically during receptor activation, enabling coordinated metabolic regulation.\u003c\/p\u003e\n\u003cp\u003eSynergistic Regulation of Gastrointestinal Function\u003c\/p\u003e\n\u003cp\u003eInfluencing Gastrointestinal Hormone Secretion: GLP-1R agonists stimulate GLP-1 secretion, while GIPR agonists regulate GIP release. These gastrointestinal hormones play crucial roles in modulating gastrointestinal motility, digestion, and absorption. By simultaneously activating both receptors, Retatrutid provides more comprehensive regulation of gastrointestinal hormone secretion, thereby influencing gastrointestinal function. It may reduce rapid nutrient absorption by modulating gastric emptying rates and intestinal motility, aiding in weight and blood glucose control.\u003c\/p\u003e\n\u003cp\u003eImproving the Gastrointestinal Metabolic Environment: By regulating gastrointestinal hormone secretion, Retatrutid also enhances the metabolic environment within the gastrointestinal tract. It promotes the growth and metabolism of beneficial gut bacteria and modulates intestinal barrier function. These alterations may further influence the body's overall metabolic state. Working synergistically with effects on energy metabolism and blood glucose regulation, these mechanisms collectively contribute to the therapeutic effects against obesity and related metabolic disorders.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eWhat are the applications of Retatrutid?\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eObesity Treatment\u003c\/p\u003e\n\u003cp\u003eSignificant Weight Loss Effects: Multiple clinical trials demonstrate Retatrutid's efficacy in obesity treatment. In a Phase 2 double-blind, randomized, placebo-controlled trial by Jastreboff A M involving 338 adults, participants received weekly Retatrutid at varying doses or placebo for 48 weeks. Results showed that at week 24, the 1mg group achieved an average weight loss of 7.2%, the 4mg combination group lost 12.9%, the 8mg combination group lost 17.3%, and the 12mg group lost 17.5%, while the placebo group lost only 1.6%. By week 48, the 1mg group achieved an average weight loss of 8.7%, the 4mg combination group lost 17.1%, the 8mg combination group lost 22.8%, the 12mg group lost 24.2%, and the placebo group lost 2.1%. Among participants receiving 4mg, 8mg, and 12mg Retatrutid, 92%, 100%, and 100% achieved 5% or greater weight loss, respectively. 75%, 91%, and 93% achieved 10% or greater weight loss. and 60%, 75%, and 83% achieved 15% or greater weight loss, compared to 27%, 9%, and 2% in the placebo group. These data conclusively demonstrate Retatrutid's efficacy in weight reduction for obese patients\u003csup\u003e[4]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eType 2 Diabetes Treatment\u003c\/p\u003e\n\u003cp\u003eGlycemic Control Efficacy: Studies by Lopez D C et al. indicate Retatrutid positively impacts glycemic control in type 2 diabetes patients. In a trial involving 353 participants, Retatrutid reduced glycated hemoglobin (HbA1c) by 1.64% compared to placebo. This demonstrates Retatrutid's efficacy in lowering blood glucose levels in type 2 diabetes patients, thereby contributing to improved clinical outcomes\u003csup\u003e[7]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eCombined Mechanism Advantage: Retatrutid acts on multiple receptors, offering a unique advantage over single-receptor agonists through its combined agonist mechanism. It not only lowers blood glucose by stimulating insulin secretion but also enhances insulin sensitivity, enabling body cells to utilize insulin more effectively for comprehensive glycemic control. Its weight-reducing effects further improve metabolic status in type 2 diabetes patients, as obesity is a significant risk factor for the condition and weight loss facilitates better blood glucose management\u003cspan\u003e \u003c\/span\u003e\u003csup\u003e[5]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eTreatment of Non-Alcoholic Fatty Liver Disease\u003c\/p\u003e\n\u003cp\u003eReducing Liver Fat Content: Retatrutid demonstrated the ability to reduce liver fat content in patients with metabolic dysfunction-associated fatty liver disease (MDAFLD) and liver fat content ≥10%. In a randomized, double-blind, placebo-controlled trial, 98 participants were randomly assigned to receive weekly subcutaneous injections of Retatrutid (1mg, 4mg, 8mg, or 12mg) or placebo for 48 weeks. Results showed that at week 24, the mean change in hepatic fat content relative to baseline was -42.9% in the 1mg group, -57.0% in the 4mg group, -81.4% in the 8mg group, and -82.4% in the 12mg group, compared to +0.3% in the placebo group. These findings indicate that Retatrutid significantly reduces hepatic fat content, demonstrating potential therapeutic value for non-alcoholic fatty liver disease\u003csup\u003e[8]\u003c\/sup\u003e.\u003c\/p\u003e\n\u003cp\u003eImproving Hepatic Metabolic Function: Retatrutid enhances liver metabolic function by regulating energy and lipid metabolism. It promotes the oxidation and breakdown of hepatic fats, reduces fat accumulation in the liver, modulates inflammatory responses and oxidative stress levels within the liver, and exerts a certain inhibitory effect on the progression of NAFLD, thereby protecting patients' liver health.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eAs a triple receptor agonist of GLP-1R\/GIPR\/GCGR, Retatrutid exerts metabolic regulatory effects through a multi-target synergistic mechanism. Its effects encompass activating GLP-1R to suppress appetite and delay gastric emptying, thereby reducing energy intake; activating GIPR to enhance insulin secretion and improve insulin sensitivity; and activating GCGR to promote lipolysis and energy expenditure while regulating hepatic glucose and lipid metabolism to reduce fat accumulation. This triple synergy achieves comprehensive effects including potent glycemic control, significant weight loss, and improved lipid and hepatic fat metabolism. Its core value lies in obesity treatment, achieving dose-dependent weight reduction with a maximum 48-week loss of 24.2%. For type 2 diabetes, it effectively lowers glycated hemoglobin and improves glycemic homeostasis. In metabolic dysfunction-associated fatty liver disease, it significantly reduces hepatic fat content, demonstrating potent efficacy across multiple metabolic disorders.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eAbout The Author\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eThe above-mentioned materials are all researched, edited and compiled by Cocer Peptides.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eScientific Journal Author\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003eArun J. Sanyal is a hepatologist and researcher specializing in liver diseases, particularly non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). He is affiliated with the Virginia Commonwealth University School of Medicine, where he has been a faculty member since 1989. Sanyal has authored approximately 1,000 publications in leading journals such as Cell Metabolism, Nature Medicine, The New England Journal of Medicine, and The Lancet. His work has been cited over 104,000 times, reflecting his significant impact on the field of hepatology. He has been continuously funded by the National Institutes of Health since 1995 and is the principal investigator of four active NIH grants. Sanyal has also been recognized for his leadership in clinical research and his contributions to the development of therapeutic strategies for liver diseases. Arun J. Sanyal is listed in the reference of citation [5].\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eRelevant Citations\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003e[1] Brzozowska P, Frańczuk A, Nowińska B, Makłowicz A, Palacz KA, Lenartowicz I. Retatrutid - revolutionary recently developed GLP agonist - literature review. Quality in Sport 2024.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/api.semanticscholar.org\/CorpusID:271031379\"\u003ehttps:\/\/api.semanticscholar.org\/CorpusID:271031379\u003c\/a\u003e.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003cp\u003e[2] Doggrell SA. Retatrutid showing promise in obesity (and type 2 diabetes).\u003cspan\u003e \u003c\/span\u003e\u003cem\u003eExpert Opinion On Investigational Drugs\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e2023;\u003cspan\u003e \u003c\/span\u003e\u003cstrong\u003e32\u003c\/strong\u003e(11): 997-1001.DOI: 10.1080\/13543784.2023.2283020.\u003c\/p\u003e\n\u003cp\u003e[3] Katsi V, Koutsopoulos G, Fragoulis C, Dimitriadis K, Tsioufis K. Retatrutid—A Game Changer in Obesity Pharmacotherapy. Biomolecules 2025; 15(6).DOI: 10.3390\/biom15060796.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003cp\u003e[4] Jastreboff AM, Kaplan LM, Frías JP, et al. Triple-Hormone-Receptor Agonist Retatrutid for Obesity - A Phase 2 Trial.\u003cspan\u003e \u003c\/span\u003e\u003cem\u003eNew England Journal of Medicine\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e2023;\u003cspan\u003e \u003c\/span\u003e\u003cstrong\u003e389\u003c\/strong\u003e(6): 514-526. DOI:10.1056\/NEJMoa2301972.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003c\/div\u003e\n\u003cp\u003e[5] Sanyal AJ, Kaplan LM, Frias JP, et al. Triple hormone receptor agonist retatrutide for metabolic dysfunction-associated steatotic liver disease: a randomized phase 2a trial.\u003cspan\u003e \u003c\/span\u003e\u003cem\u003eNature Medicine\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e2024;\u003cspan\u003e \u003c\/span\u003e\u003cstrong\u003e30\u003c\/strong\u003e: 2037-2048. https:\/\/api.semanticscholar.org\/CorpusID:270378167.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003cp\u003e[6] Nicholls S, Pirro V, Lin Y, et al. Triple-hormone receptor agonist retatrutide significantly improves lipoprotein and apolipoprotein profiles in participants with obesity or overweight.\u003cspan\u003e \u003c\/span\u003e\u003cem\u003eEuropean Heart Journal\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e2024;\u003cspan\u003e \u003c\/span\u003e\u003cstrong\u003e45\u003c\/strong\u003e(Supplement_1): ehae666-ehae1501.DOI:10.1093\/eurheartj\/ehae666.1501.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003cp\u003e[7] Lopez DC, Pajimna JT, Milan MD, et al. 7792 Efficacy of Retatrutid for Weight Reduction and Its Cardiometabolic Effects Among Adults: A Systematic Review and Meta-Analysis.\u003cspan\u003e \u003c\/span\u003e\u003cem\u003eJournal of the Endocrine Society\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e2024;\u003cspan\u003e \u003c\/span\u003e\u003cstrong\u003e8\u003c\/strong\u003e(Supplement_1): bvae163-bvae749.DOI: 10.1210\/jendso\/bvae163.749.\u003c\/p\u003e\n\u003cp\u003e\u003cbr\u003e\u003c\/p\u003e\n\u003cp\u003e[8] Naeem M, Imran L, Banatwala U. Unleashing the power of retatrutide: A possible triumph over obesity and  overweight: A correspondence. Health Science Reports 2024; 7(2): e1864.DOI: 10.1002\/hsr2.1864.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eALL ARTICLES AND PRODUCT INFORMATION PROVIDED ON THIS WEBSITE ARE SOLELY FOR INFORMATION DISSEMINATION AND EDUCATIONAL PURPOSES.  \u003c\/strong\u003e\u003c\/p\u003e\n\u003cdiv id=\"location_1750667616587\" data-type=\"locations\" data-level=\"rows\"\u003e\n\n\u003cdiv class=\"backstage-stwidgets-settingwrap\" scope=\"0\" id=\"component_yPKEnHFkjZhO\"\u003e\n\n\u003cdiv class=\"sitewidget-gallery sitewidget-proddetail sitewidget-162f6be7-60af-409f-a195-fbc2d9ed0d20-20250624132610 prod_des_sitewidget-162f6be7-60af-409f-a195-fbc2d9ed0d20-20250624132610\"\u003e\n\n\u003cdiv class=\"sitewidget-bd\"\u003e\n\n\u003cdiv class=\"detial-cont-divsions detial-cont-prodescription detial-cont-prodescription_pc prod_floating_mt\"\u003e\n\n\u003cdiv class=\"prod_describe_new3\" id=\"prod_describe_new_3\"\u003e\n\n\u003cdiv class=\"prod_describe_new_content\"\u003e\n\n\u003cdiv class=\"prodDetail-editor-container sliderTable\"\u003e\n\n\u003cp\u003eThe products provided on this website are intended exclusively for in vitro research. In vitro research (Latin: *in glass*, meaning in glassware) is conducted outside the human body. These products are not pharmaceuticals, have not been approved by the U.S. Food and Drug Administration (FDA), and must not be used to prevent, treat, or cure any medical condition, disease, or ailment. It is strictly prohibited by law to introduce these products into the human or animal body in any form.\u003c\/p\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\u003cdiv class=\"prod_describe_new3\" id=\"prod_describe_new_4\"\u003e\n\n\u003cdiv class=\"prod_describe_new_content\"\u003e\n\n\u003cdiv class=\"prodDetail-editor-container sliderTable\"\u003e\u003cbr\u003e\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n\n\n\u003c\/div\u003e\n","brand":"我的商店","offers":[{"title":"Default Title","offer_id":53267677937888,"sku":null,"price":480.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0813\/1759\/3312\/files\/1d345569-0894-41a5-b99a-487ff0caf410.png?v=1782900873","url":"https:\/\/zqzaq0-p8.myshopify.com\/en\/products\/retatrutid-40mg","provider":"COCER      PEPTIOES","version":"1.0","type":"link"}