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
Sources: ClinicalTrials.gov, YuYu Pharma

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Vascular disordersThrombosis✓ Approved

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PubMedZhongguo yi liao qi xie za zhi = Chinese journal of medical instrumentation2026-10-13

[Mitigation Strategies and Evaluation Methods for Lipemia Interference in In Vitro Diagnostic Products].

Ji Yurong Y, Yin Xiaofan X

Lipemia interference resistance constitutes a critical performance indicator in the design and development of in vitro diagnostic products. In this article, the causes of lipemic samples and their interference pathways are briefly introduced; currently available common strategies employed to counteract lipemia interference have been summarized, including widely accepted approaches such as ultracentrifugation and sample dilution, as well as recently implemented techniques like reagent formulation modification and measurement procedure optimization. Furthermore, based on the requirements outlined in the latest publication of the Clinical and Laboratory Standards Institute (CLSI) EP07 Interference Testing in Clinical Chemistry and the pharmaceutical industry standard of the People's Republic of China YY/T 1789.5 - 2023 Performance Evaluation Methods for In Vitro Diagnostic Test Systems - Part 5: Analytical Specificity, the standardized evaluation methods for lipemia interference are systematically discussed.

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PubMedZhongguo yi liao qi xie za zhi = Chinese journal of medical instrumentation2026-10-13

[Research on Quality Control Testing Methods for Laparoscopic Surgical Robots].

Lu Heqing H, Liao Yuan Y, Zheng Jiaxin J, Yan Hao H et al.

To address the lack of quality and safety evaluation criteria and the inconsistency of testing methods in the clinical application of laparoscopic surgical robots, this study developed a scientific and operable testing method system based on a four-dimensional framework of "device appearance and function-electrical safety-image quality-robotic arm and surgical instruments". By identifying risk points of 21 core indicators, such as leakage current and horizontal/vertical resolution, and referencing standards such as YY/T 1712-2021 to determine the testing principles, the testing tools, operation steps, and limit values for each indicator were clearly defined. Multi-center validation was conducted on seven devices of different brands in three institutions. The validation results showed that the operability of the testing methods across different devices exceeded 90%, and the qualification rate of indicators was over 77%, effectively identifying latent device quality deficiencies. This system addresses a critical gap in the applied quality evaluation of laparoscopic surgical robots, providing standardized tools for hospital acceptance, daily quality control, and health supervision, and promoting the industrialization of medical devices and the standardization of the industry.

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PubMedMicrobiological research2026-10-09

The gut-pancreas axis in chronic pancreatitis: Microbiota-endogenous GLP-1 interactions and candidate repair pathways.

Fan Zhengyang Z, Chen Yonghao Y, Li Yuan Y, Dong Yanbin Y et al.

Chronic pancreatitis (CP) is a progressive fibroinflammatory disorder with limited disease-modifying options. Human CP studies report gut microbial and intestinal-barrier alterations, predominantly in cross-sectional cohorts. This review integrates CP-specific clinical and experimental observations with mechanistic evidence from cell, rodent, and non-CP human studies. Barrier disruption can increase lipopolysaccharide exposure and engage Toll-like receptor 4-associated inflammatory and fibrogenic signaling, whereas microbial and host-derived metabolites regulate enteroendocrine L-cell secretion through defined receptor-mediated and metabolic pathways. Human glucagon-like peptide-1 (GLP-1) studies in CP show heterogeneous responses, while CP trials have not yet connected microbiota-driven GLP-1 changes to disease progression. Evidence for direct pancreatic GLP-1 receptor (GLP-1R) signaling is strongest in β cells; reported immune, stellate-cell, and exocrine effects derive largely from preclinical or pharmacological studies and should not be equated with physiological endogenous GLP-1 exposure. CP-specific animal studies reported attenuated fibrosis or improved barrier and immune endpoints after microbiota-directed interventions, whereas limited human synbiotic trials reported improvements in selected gastrointestinal or perioperative outcomes but did not assess endogenous GLP-1, microbiome engraftment, pancreatic fibrosis, or disease progression. Together, these findings support a biologically coherent and testable microbiota-metabolite-endogenous GLP-1 framework for CP, with causal direction and clinical relevance requiring longitudinal validation. Translation requires microbiome-stratified CP trials incorporating functional microbiome and metabolite profiling; basal and meal-stimulated measurements of active and total GLP-1, together with peptide YY; prespecified clinical outcomes; mediation and treatment-by-biomarker analyses; and long-term safety assessment.

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PubMedFrontiers in nutrition2026-10-09

Intermittent fasting-associated microbiome remodeling and functional modulation by Lacticaseibacillus rhamnosus HN001.

Shao Tinghui T, Liu Jin-Ming JM

The gut microbiome is a critical regulator of host metabolism, yet how intermittent fasting (IF) remodels the gut ecosystem independent of dietary composition remains unclear. This study aimed to isolate the effect of feeding rhythm on the gut microbiome and identify specific microbial taxa mediating IF-induced metabolic changes. We employed a family-based 'shared meal' model that strictly standardized dietary composition across all participants. Five healthy adults (3 males, 2 females) from a single family participated in a pilot, hypothesis-generating 4-week 16:8 IF intervention with longitudinal fecal sampling for 16S rRNA sequencing and untargeted metabolomics. To functionally test a candidate Lacticaseibacillus-associated mechanism, C57BL/6 J mice were subjected to a 1-week 16:8 IF protocol with or without daily oral supplementation of Lacticaseibacillus rhamnosus HN001. Plasma beta-hydroxybutyrate (betaOHB) and peptide YY (PYY) were measured by ELISA. IF was associated with body weight loss in humans (2.1 +/- 0.4 kg, 95% CI: 1.3 to 2.9 kg, p < 0.05) without a significant reduction in caloric intake. In the primary paired genus-level DESeq2 analysis accounting for participant identity, no genus remained significant after false-discovery-rate correction, although Lacticaseibacillus showed a directional decrease after IF, consistent in direction with the original exploratory unpaired analysis. Predicted microbial functional and fecal metabolomic changes were consistent with altered microbial energy metabolism. In mice, IF significantly elevated plasma betaOHB (p = 0.0046) and reduced body weight, whereas HN001 supplementation reversed these IF-associated effects under the conditions tested. In this pilot, hypothesis-generating human cohort, IF was associated with coordinated microbiome and metabolomic remodeling, including a directional Lacticaseibacillus signal that motivated subsequent functional testing. In mice, L. rhamnosus HN001 supplementation reversed IF-associated weight loss and ketosis, supporting the functional plausibility of a Lacticaseibacillus-associated mechanism. The human observations require confirmation in larger, independent cohorts with time-matched non-fasting controls and species-resolved microbiome measurements.

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PubMedFrontiers in cellular and infection microbiology2026-10-07

Microbiota-mediated gut-brain communication following whey protein supplementation and resistance training: current evidence linking gastrointestinal function and cognitive health.

Li Hao H, Zheng Jiaxin J, Zhang Guanqun G, Dong Xiyue X et al.

Whey protein supplementation in conjunction with resistance training (RT) has emerged as a promising strategy that may modulate microbiota-mediated gut-brain communication, with potential implications for gastrointestinal (GI) function and cognitive health. Evidence from both preclinical and clinical studies suggests that whey protein supplementation and exercise, including RT, may influence gut microbial composition and function through changes in substrate availability, intestinal physiology, and host-microbe interactions. Whey protein supplementation has been associated with source-dependent changes in gut microbial communities, including alterations in the abundance of Bacteroidetes, Bifidobacterium, and butyrate-producing taxa, whereas exercise particularly aerobic exercise, with more limited evidence for RT-has been associated with greater microbial diversity and an increased abundance of short-chain fatty acids (SCFAs)-producing bacteria. Although direct evidence evaluating the combined effects of whey protein supplementation and RT remains limited, available findings suggest that their combination may influence microbial metabolic activity in addition to microbial composition. Microbiota-derived metabolites, particularly SCFAs, together with exercise- and whey protein-induced changes in gut hormone secretion, including glucagon-like peptide-1, peptide YY, and cholecystokinin, may represent plausible mechanistic links between the GI tract and the central nervous system. These pathways may contribute to the regulation of intestinal barrier integrity, neuroendocrine communication, immune responses, and neuroplasticity. Experimental evidence further suggests that whey protein supplementation combined with exercise, including RT, may contribute to reduced oxidative stress and neuroinflammation and may support brain-derived neurotrophic factor signaling; however, direct evidence linking microbiota-mediated changes to cognitive outcomes in combined intervention studies remains scarce. Nevertheless, findings remain heterogeneous because of differences in protein dosage, exercise protocols, intervention duration, study populations, and individual microbiome variability. Overall, current evidence supports the biological plausibility of microbiota-mediated gut-brain communication as a potential mechanism underlying the effects of whey protein supplementation and RT; however, well-designed human studies directly evaluating gut microbiota, gut-brain signaling, and cognitive outcomes are needed to confirm these proposed relationships.

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PubMedACS pharmacology & translational science2026-10-04

Neuropeptide Y Receptor Binding Profiles of Endogenous Ligands in the Presence and Absence of Sodium: A Panoramic View.

Gattor Albert O AO, Schettler Franziska F, Erl Julia J, Brunner Thomas T et al.

Neuropeptide Y (NPY) receptors (YRs) play a key regulatory role in essential human physiological processes such as bone metabolism, feeding, anxiolysis, and pain modulation, making them potential therapeutic targets. Nonetheless, radiochemical ligand binding studies needed for the development of therapeutics actings at YRs, have been conducted inconsistently in the presence or absence of sodium, the latter representing a nonphysiological-like condition that may lead to inaccurate interpretations. As such, this study aimed to provide an in-depth overview of the binding affinities of endogenous YR agonists, namely NPY, peptide YY (PYY), and pancreatic polypeptide (PP), to the various YR subtypes, Y1R, Y2R, Y4R, and Y5R, in the presence and absence of sodium using recently developed tritium-labeled radioligands. Additionally, YR subtype-selective antagonists, BIBP3226 (Y1), JNJ31020028 and BIIE0246 (Y2), UR-MK188 (Y4), and CGP71683A (Y5), were studied. Significant differences in YR binding of the agonists, observed for Y1R, Y4R and Y5R binding, were indicated by higher binding affinities in the absence of sodium. The effect was most pronounced for Y1R binding of PP (ca. 100-fold difference in binding affinity). While Y2R binding of the Y2R antagonist BIIE0246 and Y4R binding of the putative Y4R antagonist UR-MK188 were not significantly influenced, a significantly decreased binding affinity was observed for the antagonists BIBP3226 (Y1R) and CGP71683 (Y5R) for binding under sodium-free conditions compared to the sodium-containing buffer. Overall, the determined YR binding affinities were largely consistent with literature data. Findings from this study confirmed sodium's allosteric modulation on YR agonist binding, although this modulatory effect was shown to be dependent on the type of ligand bound.

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