Drug Database
YY

YY-3110 (YY 3110 / YY3110)

✓ Approved

YuYu Pharma · Small Molecule · Small Molecule

What is YY-3110?

YY-3110 is a small molecule developed by YuYu Pharma. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesYY 3110, YY3110
CompanyYuYu Pharma
Drug ClassSmall Molecule
RouteUnknown
StatusApproved

Therapeutic Indications

YY-3110 is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

Related Research Articles

PubMedDiabetologia2026-05-24

A randomised clinical trial testing the safety of and metabolic responses to short-term duodenal infusion of recombinant RORDEP1 in healthy men.

Gæde Joachim J, Fan Yong Y, Lyu Liwei L, Gasbjerg Lærke Smidt LS et al.

RUMTOR-derived peptides (RORDEPs) 1 and 2 are polypeptides synthesised by specific strains of the human gut commensal Ruminococcus torques. Preclinical studies have shown that RORDEPs lower blood glucose via an impact on plasma incretins and an improvement of hepatic insulin sensitivity. In a randomised, placebo-controlled, crossover trial, we here explore the safety and tolerability of, as well as any metabolic responses to, a duodenal infusion of recombinant RORDEP1 (r-RORDEP1) given to healthy men after oral intake of a liquid mixed meal. Seventeen healthy, normal-weight men between 18 and 35 years of age were randomised through block randomisation to receive either r-RORDEP1 or placebo as the initial intervention at Gentofte Hospital, Denmark. Exclusion criteria were use of any form of medication, use of antibiotics during the 3 months before intervention, lactose intolerance, smoking, alcohol or drug abuse, or the use of probiotics or creatine as dietary supplements during the study period. Blocks were created prior to trial initiation. Both participants and investigators were blinded to treatment. Following intake of a standardised liquid meal, r-RORDEP1 was given via a naso-duodenal tube as an initial bolus of 0.0108 mg/kg body weight followed by a continuous infusion of 0.25 µg kg-1 min-1 for 170 min. Primary outcomes were changes in plasma concentrations of incretins and peptide YY, while secondary endpoints were safety and tolerability, and changes in plasma insulin, C-peptide and glucose. All 17 participants completed the trial. Duodenal infusion of r-RORDEP1 was well tolerated and without changes in biochemical measures of haematological, liver or renal functions. Compared with placebo, the bolus of r-RORDEP1 induced an early (at 15 or 30 min) rise in plasma glucagon-like peptide-1, insulin and C-peptide (q=0.001, q=0.001 and q=0.003, respectively) and a decline in plasma gastric inhibitory polypeptide and glucose (q=0.02 and q=0.006, respectively), while also increasing whole-body insulin sensitivity as measured with the Matsuda index of insulin sensitivity (p=0.049). Short-term duodenal infusion of r-RORDEP1 is safe and well tolerated and elicits changes in plasma incretins, insulin and glucose, and a measure of whole-body insulin sensitivity, aligning with findings in rodents, supporting the hypothesis that RORDEPs hold a role in impacting host metabolism. ClinicalTrials.gov NCT06923839 FUNDING: EFSD/Lilly European Diabetes Research Programme 2021, RUCILP F-19235-01-64 - NNF21SA0070428 grant and NNF23SA0084103 grant, the latter two from the Novo Nordisk Foundation.

PubMedMetabolism: clinical and experimental2026-05-22

Gut-liver metabolic and enterohormonal remodeling drives progression from metabolic dysfunction-associated steatotic liver disease to steatohepatitis.

Rivas Jaclyn A JA, Murphy Alexandria C AC, Prasad Praveena P, Yahia Mahmoud S MS et al.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic liver disease that can progress to metabolic dysfunction-associated steatohepatitis (MASH), a more severe form characterized by inflammation, hepatocyte injury, and fibrosis. Although the gut-liver axis is implicated in disease progression, stage-specific changes in gut-derived metabolites, lipids, and enteroendocrine signaling remain unclear. This study investigated metabolic, lipidomic, and enteroendocrine alterations during MASLD-to-MASH progression. Male C57BL/6NTac mice were fed a modified Amylin liver NASH high-fat diet for 16 weeks to induce MASLD or 29 weeks to induce MASH, age-matched chow-fed mice served as controls. Liver, colon, and stool underwent untargeted metabolomics and lipidomics. Plasma hormones and cytokines were measured by multiplex assay and ELISA. Histology, immunofluorescence, disease-signature enrichment, cross-species network analysis, and organoid differentiation assays were used to assess tissue pathology and signaling pathways. The high-fat diet produced histologically confirmed MASLD and MASH at 16 and 29 weeks, respectively. Cholic acid was elevated across liver, colon, and stool in both stages. MASLD was associated with increased circulating glucagon-like peptide-1, glucose-dependent insulinotropic polypeptide, and peptide YY, which correlated with colonic cholic acid as well as increased colonic TGR5 expression, whereas these changes were absent in MASH. MASH showed broader metabolic and lipid remodeling, elevated tumor necrosis factor and interleukin-6, impaired enteroendocrine differentiation markers, and increased hepatic serotonin colocalized with fibronectin. MASLD-to-MASH progression involves stage-specific gut-liver metabolic remodeling, loss of enteroendocrine responsiveness, and hepatic serotonergic-fibrotic signaling.

PubMedFrontiers in nutrition2026-05-21

The collapse of the food matrix: how ultra-processed foods impact satiety and metabolism by altering physical structure beyond nutrient composition.

Wang Xinna X, Chen Hang H, Xu Yan Y, Xu Qiaoli Q et al.

The global consumption of ultra-processed foods (UPFs) is strongly associated with the prevalence of non-communicable diseases (NCDs). This link has traditionally been attributed to their poor nutritional profiles. However, evidence shows that even when nutrient-matched, UPFs promote excess energy intake and weight gain, suggesting a pathogenic mechanism beyond their chemical composition. This review proposes a central conceptual framework: the core threat of UPFs to health may originate profoundly from the industrial collapse of their physical "food matrix." While evidence-informed, this framework remains a conceptual proposition requiring further causal validation. We hypothesize that this structural disintegration triggers a proposed top-down cascade of dysregulation. In the oral phase, a soft matrix accelerates eating rates by reducing chewing requirements, thereby weakening early satiety signals. In the gastrointestinal tract, the excessively rapid absorption of nutrients suppresses the secretion of distal gut satiety hormones, such as glucagon-like peptide-1 (GLP-1) and peptide YY (PYY). This supraphysiological nutrient flux imposes a significant challenge on core metabolic organs, driving insulin resistance and hepatic de novo lipogenesis. Ultimately, the impoverished matrix leads to gut microbiota imbalance, compromised intestinal barrier function, and low-grade systemic chronic inflammation. In conclusion, the integrity of the food matrix is an indispensable dimension for evaluating the health value of food. This paper calls for a fundamental shift in perspective within nutritional science and public health policy: from focusing solely on "what is in our food" to equally considering "what has been done to our food."

PubMedScientific reports2026-05-20

Gut hormones in POTS and their relation to hemodynamic parameters and gastrointestinal symptoms.

Tufvesson Hanna H, Roth Bodil B, Johansson Madeleine M, Hamrefors Viktor V et al.

Postural orthostatic tachycardia syndrome (POTS) is associated with multiple autonomic symptoms, including gastrointestinal (GI) complaints, and has been linked to insulin resistance. We aimed to explore HbA1c, circulating metabolic hormones (insulin, C-peptide, GIP, GLP-1, glucagon, leptin, and peptide YY) and cortisol, and their associations with hemodynamic parameters and GI symptoms in POTS. Two POTS cohorts were studied and compared with matched controls. In the fasting cohort, blood samples were drawn in 42 patients and 41 controls, followed by active standing tests with measurement of pulse and blood pressure (BP) in supine and standing positions. In the non-fasting cohort, questionnaires assessed GI symptoms and HbA1c was measured in 43 patients and 52 controls. Fasting C-peptide and insulin levels correlated with BP in POTS (q = 0.002) but not in controls. Fasting insulin tended to be higher in POTS but was not statistically significant after adjustment for BMI (β = 6.85; 95% CI: -1.04-14.74; p = 0.085). Morning cortisol was comparable between groups. In the non-fasting cohort, HbA1c and metabolic hormones were comparable between groups, with no associations with GI symptoms. Together, these findings suggest a potential link between insulin-related pathways and BP regulation in POTS. Future studies are warranted to further investigate insulin dynamics in POTS.

PubMedJournal of genetics and genomics = Yi chuan xue bao2026-05-16

A duplicated female pathway gene figla-like evolves as the male sex-determining gene in tilapia.

Xiao Hesheng H, Wang Jingrong J, Niu Yuhan Y, Yan Shuo S et al.

As the largest group of vertebrates, fish exhibit frequent turnover of sex-determining (SD) genes. Here, we assemble a chromosome-level YY red tilapia genome and identify figla-like (figlal) as the SD gene on tilapia linkage group (LG) 1. Integrative phylogenetic and genomic evidence suggests that figlal originated from a tilapia-specific duplication and transposition of the ancestral bHLH family gene figla from LG12 to LG1. Fluorescence in situ hybridization reveals expression divergence between figla and figlal, with figla expressed in female oocytes and figlal expressed in male gonadal somatic cells during early gonadal differentiation. The shift in expression after duplication might be driven by the insertion of cis-regulatory elements mediated by transposable elements. Knockout of figlal in XY fish results in male-to-female sex reversal as indicated by ovarian morphology, down-regulation of the male pathway gene dmrt1, and up-regulation of the female pathway gene cyp19a1a in the gonads. In contrast, overexpression of figlal in XX fish induces female-to-male sex reversal. These findings implicate figlal as an SD gene on tilapia LG1 and reveal the history of a unique evolutionary innovation in which a female oocyte gene evolved into a male SD gene via duplication, transposition, and cis-regulatory rewiring.

PubMedThe journal of evidence-based dental practice2026-05-12

ALVEOLAR RIDGE PRESERVATION AT MOLAR EXTRACTION SITES MAY LESSEN RIDGE CHANGES AND AUGMENTATION NEEDS.

Kumar Satish S

Wei YP, Han ZY, Hu WJ, Zhang HY, Ren YY, Xu T, Chung KH. Alveolar ridge preservation at molar extraction sites: a systematic review and meta-analysis. J Evid Based Dent Pract. 2025;25(1):102074. Study supported in part by Capital's Funds for Health Improvement and Research (2022-2-4103), and Clinical Research Foundation of Peking University School and Hospital of Stomatology (PKUSS-2023CRF505). Systematic review with meta-analysis of data.

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