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YY-3130 (YY 3130 / YY3130)

✓ Approved

YuYu Pharma · 小分子 · 小分子

什么是 YY-3130？

YY-3130 是一种小分子，由YuYu Pharma研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名YY 3130, YY3130
公司YuYu Pharma
药物类别小分子
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, YuYu Pharma

治疗适应症

YY-3130 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved

相关研究文献

PubMedMolecular nutrition & food research2026-07-27

Intermittent Fasting Amplifies Gut-Endocrine Axis Responses to Senna alexandrina Supplementation in Obese Rats.

Fulyani Faizah F, Widayanti Iftitan Setya IS, Bestari Salwa Alifa SA, Batubara Lusiana L et al.

Obesity induced by high‑fat, high‑sucrose diets (HFSD) remains a major global health challenge, disrupting lipid metabolism, glucose homeostasis, and gut microbial balance. These disturbances underscore the need for safe interventions capable of restoring metabolic regulation. Senna alexandrina (SA), traditionally used for weight reduction, has recently been shown to modulate the gut microbiota beyond its laxative effects. To enhance efficacy while minimizing adverse outcomes, this study investigated the effects of a low and safe dose of SA combined with intermittent fasting (IF), a strategy that reshapes nutrient availability and microbial dynamics. HFSD‑induced obese rats were treated for four weeks with SA leaf powder (300 mg/kg/day), IF, or both. Bioactive constituents of SA were characterized using LC‑HRMS, alongside systematic evaluation of physiological and metabolic parameters-including adiposity, morphometry, lipid profiles, insulin sensitivity markers, and gut-endocrine axis indicators. SA supplementation showed improvements across all parameters, surpassing those achieved with IF alone. Importantly, the combined intervention (SA+IF) yielded complementary benefits, notably enhancing GLUT4 expression, short‑chain fatty acid (SCFA) production, peptide YY (PYY) secretion, and reducing the Firmicutes/Bacteroidetes ratio. These findings highlight the complementary roles of SA and IF in metabolic regulation, providing experimental evidence for a potential dietary approach to mitigate obesity‑related dysfunction.

PMID 42504494
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PubMedJournal of neurogastroenterology and motility2026-07-27

Possible Mechanisms Underlying the Effects of Fecal Microbiota Transplantation in Patients With Irritable Bowel Syndrome.

El-Salhy Magdy M, Skarvatun Tora T, Hoff Dag Arne Lihaug DAL, Lunding Johan J et al.

: This study aims to identify the mechanisms underlying the effects of fecal microbiota transplantation (FMT). : This study investigated 93 patients included in our previous clinical trial: 24 received 30 g of their own feces (placebo group), while 47 and 22 received 30 g and 60 g of donor feces, respectively. The patients underwent sigmoidoscopy with biopsies, provided fecal samples, and completed questionnaires to assess irritable bowel syndrome (IBS) symptoms, fatigue, and quality of life at the baseline and at 1 month following FMT. The biopsy samples were immunostained for Musashi-1, neurogenin-3, and enteroendocrine and immune cells. The cell densities were quantified by computerized image analysis. Fecal short-chain fatty acids (SCFAs) were measured by gas chromatography, and fecal bacteria were measured by 16S ribosomal RNA polymerase chain reaction DNA amplification. : The densities of stem cells, enteroendocrine cell progenitors, serotonin, glucagon-like peptide 1, and peptide YY (PYY) cells increased following FMT in the 30-g and 60-g treated groups but not in the placebo group, and they were inversely correlated with both IBS symptoms and fatigue. The densities of submucosal immune cells and mast cells decreased following FMT in the 30-g and 60-g treated groups but not in the placebo group, and they were correlated with IBS symptoms and fatigue. The fecal level of butyric acid increased in patients treated with donor feces, and this was inversely correlated with IBS symptoms and fatigue. : Stem cells, enteroendocrine progenitors, serotonin, and glucagon-like peptide 1 as well as low-grade inflammation may play roles in IBS symptom manifestations. The effects of FMT are probably due to the amelioration of these abnormalities.

PMID 42504661
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PubMedFish physiology and biochemistry2026-07-25

Production of YY super-males in Pseudobagrus ussuriensis using estradiol-induced XY pseudo-females.

Pan Zhengjun Z, Li Shuchu S, Li Xiaorui X, Tang Tingting T et al.

The Ussuri catfish Pseudobagrus ussuriensis belongs to the XY sex-determination system of male heterogamy, exhibiting typical male-biased dimorphism during growth and development. Therefore, all-male breeding possesses substantial economic significance. It is fundamental to all-male breeding to obtain XY pseudo-female and YY super-male fish. In this study, fry (6 days post-hatching, 2-3 mm total body length) were treated with 17-β estradiol, at graded doses of 50, 100, 150, and 200 µg/L for 40 days to induce sex reversal. After treatment, XY pseudo-females were screened using male-specific molecular markers. Upon reaching sexual maturity, XY pseudo-females were mated with XY males by artificial insemination. After 1 year of rearing, YY super-males were identified from a mixed filial population. Subsequently, gonadal histological examination of XY pseudo-females and YY super-males was conducted. The results indicated that XY pseudo-females were produced across all four E2 concentrations. Higher rates of sex reversal and survival could be achieved under the treatment of 150 µg/L E2. The absolute and relative fecundity of XY pseudo-female fish were not significantly different from those of XX female fish. The proportion of YY super-male fish ranged between 9.32 and 16.59%, which was considerably lower than 25%. Mating experiments and histological examination of gonads indicated that XY pseudo-females and YY super-males were viable and fertile. In conclusion, this study demonstrates the breeding of all-male Ussuri catfish to produce YY super-male fish, adding a new strain to enhance the aquaculture production.

PMID 42501161
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PubMedThe Journal of biological chemistry2026-07-25

A biosensor platform for scalable and live detection of PYY hormone production from enteroendocrine cells with single-event resolution.

Hirdaramani Aanya A, Frost Gary G, Hanyaloglu Aylin C AC

Peptide YY (PYY) comprises the secretory repertoire of enteroendocrine L-cells alongside glucagon-like peptide-1 (GLP-1), and positively modulates postprandial satiety, digestion mechanics, and regeneration of the intestinal epithelium. Whereas immortalised GLP-1-secreting human L-cell models support pre-clinical drug discovery, comparable human lines that robustly secrete PYY are lacking, hindering mechanistic studies of its release. We present a biosensor for detection of PYY production and secretion from human enteroendocrine cells in vitro. Guided by in silico structural prediction, we engineer a superecliptic phluorin (SEP)-tagged PYY, SEP-PYY, that engages native hormone processing machinery and is responsive to canonical nutrient stimuli when expressed in a human enteroendocrine-like cell line, NCI-H716. SEP-PYY production and secretion can be measured by flow cytometry and spectrofluorometric plate readouts respectively, methods with superior time- and cost-efficacy to current hormone detection methods. Leveraging the pH sensitivity of SEP, we use this biosensor in detection of single-event hormone exocytosis by total internal reflection microscopy. Finally, we demonstrate the application of our platform in screening ligands of metabolite-sensing G-protein coupled receptors that drive SEP-PYY secretion, supporting discovery of druggable and nutrient-driven pathways in metabolic disease.

PMID 42497992
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PubMedNature metabolism2026-07-25

Distinct brain regions mediate regulation of food intake in response to GIPR agonism or antagonism.

Lewis Jo Edward JE, Montaner Mireia M, Nuzzaci Danae D, James-Okoro Paula-Peace PP et al.

The development of dual agonists for the glucagon-like peptide-1 receptor (GLP-1R) and glucose-dependent insulinotropic polypeptide receptor (GIPR) has been a landmark moment in the treatment of type 2 diabetes and obesity. However, for reasons that are incompletely understood, in preclinical and clinical studies, adding either a GIPR agonist or GIPR antagonist to GLP-1R agonism causes additional weight loss1. Here we show that distinct brain regions mediate the appetite-suppressing effects of GIPR agonists and the synergistic weight loss effects conferred by GIPR antagonists. We knock out Gipr in either the area postrema (AP) or hypothalamus of mice (GiprAP-KO and Giprhypo-KO, respectively) and compare body weight and food intake responses to GIPR agonists and antagonists, alone and in combination with the GLP-1R agonist liraglutide. GiprAP-KO mice exhibit partial protection against diet-induced obesity, reduced responsiveness to the appetite-suppressing effects of acyl-GIP and a reduced ability of acyl-GIP to prevent avoidance triggered by peptide YY. Weight loss effects of liraglutide are comparable in GiprAP-KO and control mice, and the co-administration of a GIPR antagonist peptide causes similar additional weight loss in both groups. Giprhypo-KO mice, by contrast, exhibit normal appetite suppression by acyl-GIP but enhanced weight loss on liraglutide compared with control mice. Giprhypo-KO also abolishes the synergistic effect of a GIPR antagonist when combined with liraglutide-an effect that is not mediated by nucleus tractus solitarius preproglucagon neurons. GIPR antagonism and Giprhypo-KO also sensitise to cagrilintide-induced weight loss. Overall, our results suggest that the AP is responsible for the appetite-suppressing effects of GIPR agonism but that GIP receptors in the hypothalamus underlie the ability of GIPR antagonism to enhance the weight loss effects of GLP-1R and amylin receptor agonists.

PMID 42498824
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PubMedThe Journal of clinical endocrinology and metabolism2026-07-24

Circulating levels of PYY are increased in individuals with bile acid diarrhoea.

Lange Andreas H AH, Kårhus Martin L ML, Bannon Christopher C, Forman Julie J et al.

Bile acid diarrhoea (BAD) is a chronic disease caused by a disturbance of the enterohepatic circulation resulting in an abundance of bile acids in the colon, which in turn causes diarrhoea. Since bile acids stimulate the secretion of the hormone peptide YY (PYY), we investigated PYY levels in plasma samples from earlier studies enrolling patients with BAD and healthy volunteers. We analysed total PYY in 1) a case-control study comparing individuals with BAD with matched healthy controls during acute administration of the bile acid sequestrant colesevelam and placebo; 2) a randomised controlled trial comparing the treatment effects of colesevelam and the glucagon-like peptide 1 (GLP-1) analogue liraglutide on bowel movements in individuals with BAD; and 3) a sequestrant study investigating the effect of treatment cessation in patients with BAD. We also investigated the PYY/GLP-1 ratios along the intestines of healthy individuals based on mRNA expression and immunohistochemistry. Individuals with BAD had higher fasting plasma PYY levels compared with controls but similar postprandial increments in the two groups. Symptom-alleviating treatment of BAD with sequestrants or liraglutide resulted in a decline of fasting PYY levels. Fasting PYY levels correlated positively with 7α-hydroxy-4-cholesten-3-one (C4) and plasma total bile acids. Finally, the PYY/GLP-1 ratio increased along the intestine with the highest ratios observed in the colon. Collectively, these results suggest a role for PYY as a marker for BAD pathophysiology and warrant further studies into the role of PYY in BAD and other diarrhoeal diseases.

PMID 42496159
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