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

Related Research Articles

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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PubMedJournal of integrative medicine2026-07-24

Periplocin targets STAT3 to suppress MYC expression and inhibit multiple myeloma cell proliferation.

Wei Rong-Fang RF, Chen Jing-Xian JX, Lai Shu-Ping SP, Chen Zi-Ang ZA et al.

Periplocin, a bioactive component derived from the traditional Chinese medicinal herb Cortex periplocae, has recently emerged as a promising agent for cancer treatment. However, its mode of action, particularly in the context of multiple myeloma (MM), remains poorly characterized. This study investigates the antitumor efficacy of periplocin against MM and elucidates its underlying molecular mechanisms. Cell viability was assessed using the cell counting kit-8 assay, while flow cytometry was used to analyze cell cycle distribution and apoptosis rates. The in vivo antitumor effect of periplocin was validated in a murine MM xenograft model. RNA sequencing (RNA-seq) analyses, network pharmacology, molecular docking and cellular thermal shift assay (CETSA) were used to identify potential targets and signaling pathways of periplocin in treating MM. The Gene Expression Profiling database was used to evaluate the correlation between candidate gene expression and survival outcomes in MM patients. A dual-luciferase reporter assay was used to evaluate transcriptional activity, and CUT&Tag polymerase chain reaction (PCR) was used to detect the effect of periplocin on the binding of signal transducer and activator of transcription 3 (STAT3) protein to the Myc proto-oncogene protein (MYC) promoter region. The protein expressions were explored via Western blotting analysis. Periplocin exhibited encouraging anti-MM activity in both cellular and animal models. Periplocin induced MM cell apoptosis and cell cycle blockade. Periplocin prevented the JAK2/STAT3/AKT/mTOR signaling cascade from being activated, impeding MM cell proliferation. Molecular docking and CETSA showed the interaction between periplocin and STAT3. RNA-seq analysis showed that periplocin regulated STAT3-mediated expression of MYC, whose high expression was closely related to poor prognosis in MM. Moreover, the dual-luciferase reporter assay showed that periplocin significantly suppressed STAT3 transcriptional activity. The CUT&Tag PCR results revealed that periplocin effectively inhibited the binding of STAT3 to the MYC promoter DNA region. Periplocin downregulated MYC expression. Periplocin targets STAT3, suppressing MYC expression and leading to the inhibition of MM cell proliferation; this highlights its promise as a novel treatment option for MM. Please cite this article as: Wei RF, Chen JX, Lai SP, Chen ZA, Zhou YY, Liao YP, Chen Y. Periplocin targets STAT3 to suppress MYC expression and inhibit multiple myeloma cell proliferation. J Integr Med. 2026; Epub ahead of print.

PMID 42493383
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PubMedBiologia futura2026-07-19

Achieving monosex male tilapia: a critical review of hormonal, biodegradable and genome editing strategies.

Mehmood Maimoona M, Asad Farkhanda F, Jamal Rafia R, Nadeem Aiman A et al.

Nile tilapia culture faces significant challenges due to early maturation and uncontrolled reproduction, leading to stunted growth and overpopulation. The primary solution is producing all-male populations or sterile fish. While the synthetic androgen 17α-methyltestosterone has been the industry standard for hormonal sex reversal for decades, environmental and consumer safety concerns, including potential carcinogenicity, have driven the search for sustainable alternatives. This critical review examines the full spectrum of approaches for producing monosex male tilapia, encompassing traditional methods (manual sexing, hybridization), hormonal treatments (synthetic steroids, aromatase inhibitors), biodegradable options (plant extracts like Tribulus terrestris and Basella alba, animal by-products such as cattle and carp testes), and novel genetic strategies (YY male technology, genome editing). We highlight innovative biodegradable programs and discuss how nanoparticle-mediated drug delivery can enhance therapeutic efficacy. Furthermore, we explore how genome editing technologies like CRISPR-Cas9 offer groundbreaking potential for understanding and controlling sex determination systems. Finally, we critically evaluate these methods based on effectiveness, cost, scalability, and sustainability to guide future research and the development of more environmentally responsible practices for the tilapia aquaculture industry.

PMID 42471500
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PubMedGenome medicine2026-07-17

A short-term randomized clinical trial testing feasibility of and physiological responses to a Ruminococcus torques strain in healthy overweight humans.

Gæde Joachim J, Fan Yong Y, Lyu Liwei L, Stankevic Evelina E et al.

The human gut microbiota interacts with host biology as exemplified by the effects of the Ruminococcus torques (RT) ATCC 27756 strain-a commensal human intestinal bacterial strain that synthesizes the polypeptides RORDEP1 and RORDEP2 which in rodents improve metabolism. Motivated by the metabolic effects of the RT strain in the rodent host, we explored in a short-term double blind and placebo-controlled randomized cross-over trial the feasibility and potential physiological responses of the same bacterial strain in humans. The trial undertaken at Herlev and Gentofte Hospital, Denmark included 32 healthy overweight adults. Decided by block randomization with blocks of six, we infused either 3.1 × 1011 colony forming units of the live RT ATCC 27756 strain or placebo into the duodenum during an observation period of six hours including a two-hour oral glucose tolerance test. Insulin sensitivity measured as Matsuda Insulin Sensitivity Index was the primary endpoint. The infusion of the bacterium was safe and well-tolerated. We found no effects on the primary endpoint of the trial. Compared to placebo, short-term RT infusion induced a relative rise in plasma concentrations of glucagon-like-peptide-1 (GLP-1) and peptide YY (PYY) in parallel with a relative decline in gastric inhibitory polypeptide (GIP). These intestinal hormone responses mirrored those previously reported from studies in rats. The abundance of secondary bile acids in plasma as well as a plasma marker of bone remodeling increased after infusion of RT compared to placebo. Measures of glucose tolerance, energy expenditure, cutaneous thermography, and main markers of systemic low-grade inflammation remained unchanged. Duodenal infusion during six hours of the RT ATCC 27756 strain in healthy overweight humans shows that the bacterial strain is well tolerated, and the short-term effects on intestinal hormone release align with those previously reported in rodents. The trial is registered prospectively in ClinicalTrials.gov on 2022-06-28 with ID NCT05448274 (https://clinicaltrials.gov/study/NCT05448274?intr=ruminococcus%20torques&viewType=Card&rank=1).

PMID 42464306
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