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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Lu Fei F, Liu Lu L, Yang Peng P, Gao Hang H et al.

Knee osteoarthritis (KOA) involves interactions among whole-joint loading, tissue mechanics, and cellular responses. This study mapped the structure and temporal evolution of KOA biomechanics research using bibliometric analysis and machine-learning-assisted topic modeling. English-language articles and reviews published from 2005 to 2025 were retrieved from the Web of Science Core Collection and Scopus, merged, deduplicated, and screened. The final corpus comprised 3110 publications. Publication patterns, collaboration networks, citation structures, and keyword themes were evaluated, and non-negative matrix factorization was applied to bibliographic text to identify latent topics and their temporal distribution. Annual output increased from 37 publications in 2005 to 321 in 2025. The United States led in publication output and total citations, while the University of Melbourne was the most productive institution. Keyword analysis identified five major domains spanning mechanobiology, gait and neuromuscular control, conservative load-modifying interventions, alignment correction and reconstruction, and meniscal and ligament mechanics. The selected model comprised 19 topics. Gait and lower-limb kinematics had the largest overall share. The greatest increases in mean annual topic share from 2016-2020 to 2021-2025 involved stem cells and regenerative cartilage repair, chondrocyte mechanotransduction, and meniscal tears, extrusion, and root repair. Recent changes in topic share were strongly correlated between hard and normalized soft assignments (Spearman's ρ = 0.926). Overall, publication output increased, and topic-share patterns indicated greater relative representation of mechanobiology, regenerative repair, meniscal preservation, and alignment correction, while gait and loading research remained prominent. These findings provide a descriptive map of the field's development and changing research priorities.

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Meals are a major symptom trigger in irritable bowel syndrome (IBS), yet the endocrine steps linking luminal nutrients to pain, bloating, urgency, and altered bowel habits remain poorly defined. Early studies relied heavily on mucosal enteroendocrine cell (EEC) counts. Those observations remain informative, particularly in post-infectious IBS, but findings vary with intestinal site, bowel-habit phenotype, staining, and morphometry, and cell abundance does not measure secretory function. Human meal-challenge studies distinguish circulating concentrations from stimulus-evoked responses. In IBS with diarrhea, higher fasting and fed plasma 5-hydroxytryptamine (serotonin, 5-HT) may reflect altered handling more than a uniformly exaggerated postprandial response, whereas IBS with constipation can show impaired stimulus-evoked release. Cholecystokinin, peptide YY, motilin, ghrelin, and related peptides also vary with sex, bowel habit, and visceral sensitivity. Recent human organoid and transcriptomic studies identify distinct nutrient-sensing programs among EEC subtypes and provide a cellular framework for this heterogeneity. We integrate these findings across luminal sensing, secretion, metabolism, receptor responsiveness, and motor or sensory output. The evidence does not support a single IBS endocrine signature. Standardized nutrient challenges linked to serial hormone measurements, mucosal molecular data, and objective physiological readouts are more likely to yield reproducible and clinically testable response patterns.

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Corni Fructus water extract relieves depressive behaviors by reducing oxidative stress and neuroinflammation as well as modulating gut microbiota.

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Depression is a global public health concern with limited therapies. Traditional Chinese medicines are attractive for safety and multi-target actions. Corni Fructus water extract (CFWE) is a candidate, but its mechanisms and the main active ingredients remain unclear. A chronic unpredictable mild stress (CUMS) mouse model was established and given CFWE intervention. Depressive-like behaviors were evaluated by sucrose preference test (SPT), tail suspension test (TST), and open field test (OFT). Hippocampal histopathology was examined using H&E staining. Inflammatory and oxidative stress-related factors in the hippocampus and serum were detected using ELISA kits. RT-qPCR and Western blot measured Nrf2/HO-1 and IκBα/NF-κB pathway components. Gut microbiota and short-chain fatty acids (SCFAs) were analyzed via 16S rRNA sequencing and GC-MS. LC-MS determined the major chemical constituents of CFWE. CFWE significantly alleviated CUMS-induced depressive-like phenotypes, including preserved body weight, reduced immobility time in TST, increased sucrose preference, and greater central distance in OFT (P < 0.05 or P < 0.01). It also increased neuronal survival in hippocampal CA1/CA3 (P < 0.01), lowered pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and MDA (P < 0.05) in serum and hippocampus, and elevated CAT and SOD activities dose-dependently (P < 0.05). Mechanistically, CFWE upregulated Nrf2, HO-1, and IκBα expression, while downregulating phosphorylated NF-κB p65 expression (P < 0.05). It also restored gut microbial diversity (P < 0.05), promoted beneficial taxa (Muribaculaceae and Lactobacillus), enhanced SCFAs production, and elevated peripheral peptide YY (PYY). LC-MS analysis revealed that the main active constituents in CFWE were terpenoid glycosides, flavonoid glycosides, and organic oxygen compounds. The antidepressant-like effects of CFWE might involve activation of the Nrf2/HO-1 antioxidant pathway, suppression of the IκBα/NF-κB inflammatory response, and modulation of gut microbiota composition and SCFA metabolism, while PYY might serve as a candidate mediator in gut-brain communication.

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Obesity is increasingly recognized as a disorder of bidirectional communication among the gut microbiota, immune system, and neural circuits controlling energy balance and feeding behavior. This review examines the associations and potential mechanistic links between obesity-associated dysbiosis, chronic low-grade inflammation, and impaired appetite regulation through interconnected peripheral and central pathways. We discuss how these signals reach the central nervous system (CNS), and promote microglial and astrocytic activation, impair leptin and insulin signaling, and disrupt hypothalamic POMC and AgRP/NPY neuronal networks. We also examine how microbial metabolites and structural components influence appetite through enteroendocrine hormones, vagal afferents, blood-brain barrier (BBB) integrity, and direct actions on neural and glial cells. Particular emphasis is placed on short-chain fatty acids, tryptophan-derived metabolites, bile acids, and lipopolysaccharide, as well as their effects on glucagon-like peptide-1 (GLP-1), peptide YY (PYY), serotonergic signaling, and mesolimbic reward pathways. Together, these findings support a bidirectional framework in which diet, microbiota function, immune signaling, and neural regulation may reinforce one another during obesity progression. However, the directionality and causal relevance of many of these relationships, particularly in humans, remain incompletely understood. Clarifying these microbiota-gut-brain interactions may identify new targets for restoring appetite control and interrupting obesity progression.

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Dietary components that influence appetite-related hormones and subjective satiety may help regulate food intake. Aqueous carob (Ceratonia siliqua L.) preparations may have a role in postprandial appetite regulation. To investigate the effects of an aqueous carob preparation incorporated into a high-fat meal on postprandial appetite-related hormones and subjective satiety. An acute randomized controlled crossover trial was conducted in 20 healthy males. Participants consumed two meals of similar energy content on separate occasions: a control meal containing an orange-flavoured beverage and a test meal containing an aqueous carob preparation. Blood samples and subjective appetite ratings, assessed using visual analogue scales, were collected over a 180-minute postprandial period. Compared with the control meal, the carob meal resulted in lower subjective hunger (p = 0.011) and desire to eat (p = 0.029), and greater satisfaction (p = 0.047). Peptide YY (PYY) area under the curve (AUC) values differed between meals (p = 0.040). Following the control meal, ghrelin decreased at 30 min (p = 0.012), followed by a marked increase at 180 min (p < 0.005). The magnitude of the change in ghrelin from baseline to 180 min differed between meal conditions (p = 0.005). The findings suggest that an aqueous carob preparation may improve subjective appetite responses when consumed with a high-fat meal. Differences in PYY and ghrelin responses may contribute to these effects, although a causal relationship was not established. The acute study design and inclusion of only healthy males limit conclusions about long-term effects and applicability to other populations. Incorporating an aqueous carob preparation into a high-fat meal may favourably influence postprandial appetite and satiety regulation. Further research is needed to determine whether these effects persist over time and translate into reduced food intake.

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