Peptide United

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The living record of peptide science.

PubMed studies synced daily. Active clinical trials. Evidence updates when the science materially changes. Monthly synthesis for practitioners.

3963indexed studies
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3,963 studies
Unknown
2026

A Clinical Prediction Model for Selective NT-proBNP Testing in Hypertension.

J Clin Hypertens (Greenwich)

Anping Cai, Lin Liu, Xiangbing Yu +4 more

N-terminal pro-B-type natriuretic peptide (NT-proBNP) testing is recommended for pre-heart failure (pre-HF) screening. However, universal NT-proBNP testing is infeasible and inefficient. We analyzed data from 4642 U.S. adults with hypertension in NHANES 1999-2004. Heart stress, a biomarker-defined pre-HF state, was defined using age-specific NT-proBNP cutoffs. Multivariable logistic regression was used to identify factors associated with prevalent heart stress, and a point-based score was constructed. Model discrimination and calibration were internally validated using 1000 bootstrapped samples. Heart stress was present in 31% of individuals with hypertension. Factors associated with heart stress included older age, current smoking, prior coronary heart disease/myocardial infarction, higher systolic blood pressure, lower diastolic blood pressure, and reduced estimated glomerular filtration rate. The derivation model showed acceptable discrimination (AUC 0.71; 95% CI 0.70-0.73) and good calibration. An optimal cutoff of 6 points was identified using the Youden index and was internally validated (AUC 0.71; 95% CI 0.69-0.74). Model performance was consistent across race/ethnicity and body mass index subgroups, with relatively lower discrimination in females than in males (AUC 0.66 vs. 0.78). When stratified by a predicted heart stress probability threshold of 50%, individuals in the higher-probability group had higher cumulative risk of all-cause (hazard ratio 3.90; 95% CI 3.55-4.29) and cardiovascular mortality (hazard ratio 5.18; 95% CI 4.44-6.04) than those in the lower-probability group. These findings suggest that a simple model using readily obtainable clinical variables can help identify individuals with hypertension who are likely to have prevalent heart stress, offering a practical strategy to guide selective NT-proBNP testing.

Unknown
2026

DNA methylation inhibitor decitabine ameliorates spondyloarthritis by suppressing Th17 responses and epigenetically upregulating VIPR1 in SKG mice.

Arthritis Res Ther

Hoshiko Furusawa, Goh Murayama, Masaki Nojima +7 more

Spondyloarthritis (SpA) is a chronic inflammatory disorder characterized by enthesitis of axial and peripheral joints. Although genetic factors, bacterial infection, dysbiosis, and mechanical stress contribute to its development, the role of epigenetic regulation remains poorly understood. DNA methylation has been implicated in immune dysregulation, and the DNA methyltransferase inhibitor, decitabine (DAC), has demonstrated therapeutic effects in autoimmune disease models. This study aimed to evaluate the effect of DAC in the SpA-resembling SKG/Jcl (SKG) mouse model and elucidate the immunological mechanisms.

Unknown
2026

Changes in incretin hormone concentrations after pancreaticoduodenectomy: a systematic review and exploratory meta-analysis.

Front Endocrinol (Lausanne)

Oliwia Grząsiak-Kraj, Tomasz Kraj, Krzysztof Poznański +2 more

Pancreaticoduodenectomy (PD) removes the duodenum and proximal jejunum, alters nutrient transit, and may modify secretion of incretin hormones involved in glucose homeostasis.

Unknown
2026

Reduced serum cortisol, IGF-1, GLP-1, and T3 levels in medication-free children and adolescents with obsessive-compulsive disorder: a case-control study.

Front Psychiatry

Fatma Coşkun, Hasibe Ağır, Rukiye Esra Ildız +4 more

Obsessive-compulsive disorder (OCD) frequently emerges during childhood and adolescence and has been associated with alterations in multiple neurobiological systems. Neuroendocrine pathways involved in stress regulation, neurodevelopment, metabolic signaling, and thyroid function interact closely to influence brain circuits implicated in OCD. However, studies simultaneously examining several neuroendocrine parameters in pediatric OCD remain limited.

Unknown
2026

In ovo dexamethasone elicits an increase in ACTH-stimulated glucocorticoid release but no effects on fear behaviors in Pekin ducks.

Poult Sci

N K Wilson, J M Schober, E M Oluwagbenga +2 more

Heat stress is among the leading causes of stress to poultry during their productive life, leading to the loss of profit at each stage of production. This event can have profound impacts on a duck's physiology, leading to changes in their behavior and an increased response to future stressors. We have previously shown that breeder ducks exposed to heat stress deposit increased quantities of glucocorticoids in their eggs, and that is correlational to altered phenotype of the offspring. We sought to replicate those findings by increased glucocorticoid content in ovo without a parental heat stress (HS) event. Eggs were injected with either dexamethasone (Dex; = 100/treatment (1ug/ul]) or saline (Con = 100/treatment (0.1 mg/egg)), sealed with silicon glue and set to incubate and hatch following industry standards. Ducklings were separated into their respective groups (n = 50/treatment/pen). At 3 weeks of age, ducks were then given an adrenocorticotropic hormone (ACTH; 0.0625 mg/kg cosyntropin in 1.0 ml saline) challenge (n = 6/treatment) or control (1.0 ml saline per bird). Blood was collected at 0,1,2, and 4 h after injection. An isolation fear test was performed on the ducks at week 3.5 and novel environment test on weeks 1 and 5. Heterophil to lymphocyte ratio (HLR), ELISA for glucocorticoids, feed conversion ratio (FCR), and weekly body weights were all calculated and recorded. No significant differences were observed in FCR, body weights, or isolation fear test metrics such as latency to first vocalization. There were significant differences in circulating corticosterone in the Con-ACTH and Dex-ACTH groups each time point. The Con-ACTH had a significant (p < 0.05) increase after hour 1, and the Dex-ACTH groups showed a further significant (p < 0.05) increase above all other groups. Similar results were obtained with cortisol and HLR. The novel environment test showed only an age effect between weeks 1 and 5. Our results show that the in ovo glucocorticoids impact physiological, but not necessarily behavioral responses.

Unknown
2026

Evolutionary conservation and adaptability of cholecystokinin neuropeptide signaling in the sea cucumber Apostichopus japonicus.

BMC Biol

Huachen Liu, Hongliang Yang, Xiang Tian +2 more

Food ingestion is fundamental for animal survival and growth, with the cessation of feeding upon nutrient fulfillment being tightly regulated by a variety of satiety factors. Notably, sulfakinin/cholecystokinin (SK/CCK)-type neuropeptide signaling has been identified as an inhibitory regulator of food intake across the animal kingdom. However, its regulatory mechanism in feeding in deuterostome invertebrates remains unclear. Here, we characterized SK/CCK-type signaling in a deuterostome invertebrate, the sea cucumber Apostichopus japonicus (phylum Echinodermata).

Unknown
2026

Neonatal exposure to di-(2-ethylhexyl) phthalate (DEHP) through breastfeeding leads to dysfunction endocrine-metabolic outcomes in male rats at adulthood.

Front Endocrinol (Lausanne)

Thayná Martins Macario, Anne R Melo Santos, Natalia da Silva Lima +2 more

The increased production of industrial chemicals has led to greater human exposure to endocrine disruptors, such as diethylhexyl phthalate (DEHP). This plasticizer, widely used in hygiene products, packaging, and medical devices, does not covalently bind to polymeric materials, which facilitates its migration and subsequent entry into the human body, primarily via the oral route. In this study, we investigated the effects of DEHP exposure during the lactation period within the framework of the Developmental Origins of Health and Disease (DOHaD) concept. The experimental model utilized Wistar female rats (n=9) that were placed for mating. Litters were standardized to six male pups (n=6) each. DEHP was administered in dams via oral gavage during the lactation (post-natal day, PND 1-21) period to three groups (n=3 dams/group): vehicle, 100 mg/kg/day, and 500 mg/kg/day. After weaning, the offspring were maintained until adulthood.At PND 90, a total of nine male pups (n=3/litters/group) were randomly selected for euthanasia and analyses. At weaning (post-natal day, PND21), animals in the 500DEHP group exhibited reduced body weight and central adiposity, accompanied by increased serum insulin levels, an elevated β-cell function index (HOMA-β), and higher serum total triiodothyronine (T3) levels. By adulthood (PND90), the 500DEHP group developed a delayed obesogenic phenotype, characterized by hyperphagia and increased relative visceral white adipose tissue (vWAT) mass. This phenotype was associated with impaired leptin secretion by vWAT, resulting in reduced circulating leptin levels. Consequently, dysregulation of hypothalamic appetite control pathways was observed, marked by decreased expression of the anorexigenic neuropeptide proopiomelanocortin (POMC) and increased expression of the orexigenic neuropeptide neuropeptide Y (NPY), concomitant with reduced suppressor of cytokine signaling 3 (SOCS3) levels. Notably, elevated serum total T3 levels persisted into adulthood. In contrast, in the 100DEHP group, hypothalamic dysfunction appeared to be the primary target, evidenced by a simultaneous increase in both POMC and NPY expression. Collectively, these findings demonstrate that neonatal exposure to DEHP during lactation influences adult phenotype in a dose- dependent manner. Higher-dose exposure (500 mg/kg/day) compromises peripheral metabolic homeostasis, particularly through vWAT dysfunction and impaired leptin secretion, whereas lower-dose exposure (100 mg/kg/day) preferentially affects central regulation, suggesting dysregulation of hypothalamic neuropeptides.

Unknown
2026

A Healthy Diet Intervention Alters Food Preferences and Eating Behaviours Without Changing Appetite, Adipokines or Glucose Homoeostasis.

J Obes

Litto Tharakan, Troy Merry, Eva Liu +7 more

The study aimed to evaluate the influence of a 12-week Mediterranean dietary pattern on eating behaviours, food preferences, appetite, satiety, hunger hormones, adipokines and glucose homoeostasis.

Unknown
2026

Senescence as a regulatory mechanism in skeletal muscle repair in young mice.

Am J Physiol Cell Physiol

Amanda L Johnson, Ryan T Bevington, Gianni Parise

Senescence is broadly considered an age-related phenomenon; however, it also been implicated in normal tissue repair and wound healing. Skeletal muscle repair is a complex process that requires the coordination of several different cell populations but the role of senescence in skeletal muscle repair has yet to be fully elucidated. We hypothesize that senescence serves as a control mechanism throughout the regenerative process and the removal of senescent cells through senolytics will negatively impact the repair process in young mice. Briefly, young mice were exposed to either (a) vehicle (VEH), receiving only a cardiotoxin (CTx) injection in one hindlimb or (b) 7 days of senolytic treatment (SEN) pre-CTx and 3x/week for 4 weeks post-CTx. Dasatinib + Quercetin (D+Q) was used to selectively eliminate senescent cells. There were no significant differences between groups in functional measures such as hindlimb grip strength and cross-sectional area. eMHC+ fibers remained elevated at D28 in the SEN group. Macrophage infiltration was twice as high in the SEN group compared to VEH at D7. Satellite cell quantity and fibrotic area were significantly increased at D14 in the SEN group compared to VEH. We conclude that reducing senescent cells during muscle repair in young mice significantly altered the kinetics of muscle repair. Therefore, senescent cells may act as a regulatory mechanism in skeletal muscle to orchestrate the activity of the different cell populations involved in repair and regeneration such as immune cells, satellite cells, and fibrotic cells.

Unknown
2026

POLY-Senolytic nanoplatform for tumor-specific eradication of senescent tumor cells and mitigation of radiotherapy-induced immune resistance of cancer.

Nat Commun

Yi Lai, Shunan Zhang, Jiaxing Pan +9 more

Radiotherapy (RT) efficacy is limited by RT-induced immune resistance. Here we show that RT upregulates programmed death ligand 1 (PD-L1) on senescent tumor cells (STCs) via bromodomain-containing protein 4 (BRD4) signaling, thereby promoting immune evasion. To counter this, we develop POLY-Senolytic, a polymeric senolytic nanoparticle formed by conjugating an acid-responsive polymer to a peptide-based BRD4 PROteolysis-TArgeting Chimera via a reduction-cleavable disulfide bond. The POLY-Senolytic is activated in the acidic and reductive intracellular environment of tumor cells, leading to BRD4 degradation, suppression of RT-induced PD-L1 expression and enhanced immune clearance of STCs. Combined with RT, the POLY-Senolytic suppresses tumor growth and metastasis in orthotopic mouse models of pancreatic and breast tumors. We further engineer a β-galactosidase-responsive POLY-Tracker for real-time monitoring of senolytic therapy. Together, this study identifies an RT-driven BRD4-PD-L1 axis in STCs that promotes immune resistance and provides a practical strategy to eliminate and track them.

Unknown
2026

Correlates of serum thiamine levels among acute decompensated heart failure patients.

Cardiovasc J Afr

Busayo O Oguntola, Rasaq A Adebayo, Suraj A Ogunyemi +5 more

Acute decompensated heart failure (ADHF) contributes adversely to health-related outcomes. Anorexia, early satiety, high metabolic rates, malnutrition, advanced age, and diuretic use characterise ADHF. This necessitated evaluating the correlates of low serum thiamine levels among ADHF patients in our facility.

Unknown
2026

Steroidal response following intravenous administration of long-term frozen tetracosactide acetate in healthy Beagles.

J Vet Intern Med

Mathilde Vilcot, Nathan Docquier, Anaïs Blazy +5 more

The adrenocorticotropic hormone (ACTH) stimulation test is used to assess adrenal function. The effects of extended freezing of tetracosactide acetate (TCA), an ACTH analogue, on test performance, remain unexplored.

Unknown
2026

Combination therapy of pasireotide and pegvisomant for aggressive acromegaly with an immature PIT1-lineage PitNET.

Endocrinol Diabetes Metab Case Rep

Keiko Tomiyama, Izumi Fukuda, Shigeyuki Tahara +3 more

A 29-year-old male presented with central scotoma and was suspected of having acromegaly based on enlargement of facial features and extremities. Serum growth hormone (GH) and insulin-like growth factor 1 (IGF-1) levels were elevated to 10.14 ng/mL and 571 ng/mL (74.8 nmol/L, +5.73 SDS), respectively. Magnetic resonance imaging revealed a giant pituitary neuroendocrine tumor (PitNET) measuring 48 × 48 × 58 mm with bilateral cavernous sinus invasion and high T2-weighted signal intensity. Because of poor GH suppression during an acute octreotide test (100 μg subcutaneously; nadir GH 6.25 ng/mL, 19% reduction from baseline) and the invasive tumor phenotype, preoperative pasireotide (PAS) 40 mg every 4 weeks was initiated. After 2 months, partial tumor removal was performed via transsphenoidal surgery. Histological analysis revealed an immature PIT1-lineage PitNET with strong membranous expression of somatostatin receptor subtypes 2 and 5. Persistently elevated IGF-1 after surgery led to re-initiation of PAS (40 mg every 4 weeks, escalated to 60 mg), followed by the addition of pegvisomant (PEG) 10 mg/day because biochemical control could not be achieved. Combination therapy with PAS and PEG normalized IGF-1 and maintained radiological tumor stability during long-term follow-up. This case highlights that biochemical response to somatostatin receptor ligands does not necessarily correlate with receptor expression in invasive PitNETs. Pathological classification using transcription factors may help guide individualized treatment strategies. Combination therapy with PAS and PEG may represent an effective option for aggressive acromegaly caused by immature PIT1-lineage PitNETs.

Unknown
2026

Skeletal muscle overuse injury: pathophysiological mechanisms, molecular pathways, and rehabilitation strategies.

Front Physiol

Guoliang Wu, Na Li

Skeletal muscle overuse injury (OUI) is a load-related condition that develops when repeated mechanical loading exceeds the adaptive and reparative capacity of skeletal muscle. Unlike acute traumatic injury or delayed-onset muscle soreness after unaccustomed eccentric exercise, chronic skeletal muscle OUI is characterized by recurrent subthreshold loading, insufficient recovery, persistent low-grade inflammation, impaired regeneration, and maladaptive remodeling. This narrative review summarizes and critically appraises current evidence on the conceptual boundaries, pathophysiological mechanisms, molecular pathways, and rehabilitation strategies of skeletal muscle OUI. Particular emphasis is placed on distinguishing direct skeletal muscle evidence from indirect or extrapolative evidence derived from acute injury models, adjacent musculoskeletal disorders, disease models, or preclinical studies. Key mechanisms include myofiber microdamage, satellite-cell-mediated repair, extracellular matrix remodeling, inflammatory signaling, oxidative stress, mitochondrial dysfunction, protein turnover, and myogenic transcriptional regulation. Current management remains centered on individualized load modification, graded rehabilitation, correction of biomechanical contributors, and criteria-based return to activity. Pharmacological and physical modalities may provide adjunctive symptom control in selected cases, whereas regenerative, gene-based, wearable-sensor-based, and artificial-intelligence-assisted approaches remain emerging or experimental for chronic skeletal muscle OUI. By integrating mechanistic evidence with rehabilitation practice and evidence appraisal, this review provides a focused framework for understanding, preventing, and managing skeletal muscle OUI.

Unknown
2026

Cell sources and engineering strategies for cultured meat production: a critical comparative review.

Front Nutr

Dominika Domagała, Aleksandra Partyńska, Krzysztof Data +11 more

Meat production and ethical concerns related to animal welfare have led to an increase in research into the creation of conventional meat. These technologies rely on the isolation, multiplication, and controlled differentiation of animal cells, which can potentially reduce negative environmental impact while maintaining comparable nutritional and sensory properties. The aim of this study is to comprehensively analyze and compare selected cell types used in the production of cultured meat, such as fibroblasts, satellite cells, adipocytes, and pluripotent cells: embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs). It is important to consider the proliferative capacity, differentiation potential, suitability in scalable bioprocessing systems, and their impact on the structure and sensory properties of muscle tissue. This analysis demonstrates that no single cell type can fully replicate the complex structure of native muscle tissue. Satellite cells are responsible for the formation of muscle fibers, fibroblasts provide support through the synthesis of the extracellular matrix, and adipocytes contribute to the flavor and juiciness of the final product. Pluripotent cells differentiate into all of cell lineages, but their use is associated with regulatory and ethical considerations. This work also addresses key aspects of bioprocess engineering, such as scalability, culture conditions, and the importance of 3D cell culture and cell co-cultures in restoring tissue structure. Furthermore, regulatory, ethical, and economic issues affecting the feasibility of implementing the technology for industrial production are considered. In summary, the data presented indicate that the development of cultured meat requires an integrated approach combining appropriate cell selection, process optimization, and compliance with regulatory and ethical requirements.

Unknown
2026

Myostatin Inhibitory D‑Peptides Induce Skeletal Muscle Hypertrophy along with Alteration of Bioactive Sphingolipid Metabolism.

ACS Pharmacol Transl Sci

Katsuya Morito, Natsuki Nishikawa, Keisuke Hitachi +5 more

Myostatin inhibition is well-known as a promising strategy to induce skeletal muscle hypertrophy. Midsized peptides are currently noted as a new modality in broad drug development. Our previous studies identified a series of myostatin inhibitory peptides, including the 16-mer D-peptide inhibitor MID-35. However, the detailed pharmacological analysis of muscle growth provided by intramuscularly injected MID-35 has not been investigated. Additionally, since sphingosine 1-phosphate (S1P), one of the bioactive sphingolipids, is involved in the regulation of muscle mass, it is vital to explore whether MID-35 treatment affects the S1P metabolism. Here, we analyzed alterations induced by MID-35 administration in the tibialis anterior muscles of young, adult, and aged mice. Muscle differentiation-related markers (Pax7/Myod1/Myog) and atrophy-related markers (Trim63/Fbxo32) were robustly increased and decreased, respectively, within 3 days, and muscle weight gain first appeared 14 days later; intriguingly, the hypertrophy was sustained for 12 weeks. An increase in centralized nuclei and Pax7-positive signals in MID-35-treated muscles corroborated muscle regeneration associated with muscle satellite cells (mSCs). Additionally, changes in the bioactive sphingolipid metabolism were observed. In young and adult mice, the amount of S1P was significantly increased on day 3, suggesting that S1P may assist in the activation of the mSCs. Meanwhile, aging affects S1P metabolism, resulting in no significant increase in the S1P level in aged mice. This basic study using MID-35 newly proposes the interaction between myostatin signaling and bioactive sphingolipid metabolism in the muscle hypertrophic reaction and would accelerate further mechanistic evaluation, including the maintenance of the hypertrophic state.

Unknown
2026

Engineering a Dual-Regenerative Cascade: Injectable Hydrogel with Zn2+/l-Arg Cross-Linkers and Macrophage-Targeting Carbon Dots for Synergistic CLI Therapy.

ACS Appl Mater Interfaces

Haoran Wang, Ning Ding, Mariano Romero +4 more

Critical limb ischemia (CLI) remains refractory to current revascularization strategies due to its complex pathology. Here, we report an injectable alginate hydrogel that orchestrates a dual-pathway regenerative cascade by simultaneously reprogramming the immune microenvironment and activating direct tissue repair. The system is rationally designed by integrating two functional modules: (i) immunomodulatory carbon dots (PNS-AA@CQDs-COS) that selectively target M1 macrophages and drive them to the M2 phenotype, and (ii) intrinsically bioactive cross-linkers (Zn2+/l-Arg) that serve as sustained-release pro-regenerative signals. Critically, this dual-component architecture enables a synergistic interplay─while the carbon dots establish an anti-inflammatory microenvironment (path 1), the liberated Zn2+ and l-Arg directly activate endothelial cells and muscle satellite cells, thereby initiating coordinated vascular and myogenic regeneration (path 2). In vitro, the hydrogel significantly amplified reparative crosstalk within macrophage-endothelial/myogenic cells' cocultures. In a murine CLI model, a single injection of the hydrogel resulted in durable recovery of hindlimb perfusion (80.4% by day 14), improved motor function, and enhanced tissue repair. Mechanistic studies revealed that these benefits stem from microenvironment remodeling (M2 polarization and IL-10 upregulation) and modulation of key signaling pathways─suppressing NF-κB while potentiating PI3K/Akt/eNOS. This work presents a material-based strategy that couples immunomodulation with direct cellular activation, offering a synergistic therapeutic platform for CLI and potentially other ischemic diseases.

Unknown
2026

An Engineered Core-Satellite Magnetic Aptasensor with Built-In Calibration and Regeneration for Accurate Quantification of Oral Cancer Exosomes.

ACS Appl Mater Interfaces

Wenxi Wang, Renjie Li, Siqi Wei +6 more

Exosomes carry diverse biologically active substances that can be transferred between cells, thereby influencing physiological and pathological states of the organism. Abnormal exosome levels are closely associated with cancer. Consequently, the precise detection of exosomes holds considerable importance for noninvasive cancer diagnosis and monitoring. Nevertheless, achieving highly sensitive and consistently reproducible detection of exosomes continues to pose a significant challenge in clinical diagnostics. In this research, we developed a reusable magnetic aptamer-based surface-enhanced Raman scattering (SERS) sensor with built-in calibration for the accurate quantification of exosomes derived from oral cancer. The sensor was synthesized through a layer-by-layer assembly strategy to form an internal standard encoded core-satellite structure (NiFe2O4@PB@Ag), which was subsequently conjugated with SH-modified complementary DNA (cDNA) to form NiFe2O4@PB@Ag-cDNA. This was then hybridized with ROX-labeled aptamers (ROX: 6-carboxy-X-rhodamine) to construct the final NiFe2O4@PB@Ag-dsDNA SERS aptasensor. Magnetic-induced assembly of the sensor, combined with the surface plasmon effect, significantly improved the SERS performance, enabling dual amplification of both internal standard and target signals. This resulted in a 1.9-fold increase in signal intensity compared to the condition lacking magnetic-induced assembly. Furthermore, this SERS sensor exhibited a wide linear range for exosome detection, spanning from 5.0 × 103 to 5.0 × 1011 particles/mL, with a limit of detection (LOD) as low as 1.15 × 103 particles/mL. Finally, in clinical testing of plasma samples, the sensor reliably differentiated exosome concentrations between individuals with oral cancer and healthy controls, providing a robust and reliable platform for exosome-based liquid biopsy in clinical applications.

Unknown
2026

Semaglutide and Follow-On Peptide Therapeutics: Balancing Innovation, Regulation, and Clinical Outcomes.

Cureus

Brij Teli, Shrikant Somani, Vivek Arya +7 more

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have emerged as an important therapeutic class for the management of type 2 diabetes mellitus (T2DM) and obesity owing to their ability to improve glycemic control, promote weight loss, reduce cardiometabolic parameters, and have the added advantage of a low risk of hypoglycemia due to glucose-independent insulin secretion. Semaglutide, a long-acting GLP-1 RA developed using a semi-recombinant process, has demonstrated significant benefits across metabolic and cardiovascular outcomes. Amid the increasing need for affordable therapies, there has been a rising interest in developing synthetic peptide versions of glucagon-like peptide-1 (GLP-1)-based drugs originally produced using recombinant deoxyribonucleic acid (rDNA) technology. However, the transition from recombinant production to chemical peptide synthesis raises important considerations about regulatory pathways, manufacturing processes, and potential clinical implications. Regulatory approaches for synthetic peptides vary across regions. The European Union and the United States follow distinct frameworks, with India adopting a risk-based regulatory approach that may require extensive quality, safety, and clinical data. Manufacturing processes can influence impurity profiles, stability, and immunogenicity, potentially affecting clinical outcomes. Therefore, the approval of follow-on versions of semaglutide requires a rigorous demonstration of both quality and clinical comparability with the originator, consistent with principles applied to biosimilars. Online databases such as PubMed, Scopus, and Google Scholar were used to source relevant research articles. This narrative review aims to discuss the development of semaglutide, examine global and national regulatory perspectives on synthetic and recombinant peptides, and explore the clinical implications of manufacturing variability. It also highlights the expanding therapeutic potential of semaglutide beyond obesity and T2DM.

Unknown
2026

Real-world experience of semaglutide 2.4 mg in the US: a retrospective analysis of profiles, satisfaction, and treatment patterns in people with obesity and overweight.

Curr Med Res Opin

Yiqiao Zhang, Zhenxiang Zhao, Victoria Higgins +1 more

To characterize treatment experiences, compliance with dosing frequency, and adherence to treatment regimen, and to assess factors associated with adherence and compliance among patients with obesity or overweight (PwO) receiving semaglutide 2.4 mg for weight management.

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