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pancrelipase (Ultrase MT20 / Ultrase MT / Ultresa)

✓ Approved

Adare Pharma Solutions · PNLIP

什么是 pancrelipase？

pancrelipase 是一种治疗药物，由Adare Pharma Solutions研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Ultrase MT20, Ultrase MT, Ultresa
公司Adare Pharma Solutions
分子靶点PNLIP
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Adare Pharma Solutions

作用机制

分子靶点

pancrelipase 作用于 1 个分子靶点：

PNLIPpancreatic lipase (PL, PNLIPD)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

pancrelipase 针对 3 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
InvestigationsFaecal fat increased✓ Approved
Gastrointestinal disordersSteatorrhoea✓ Approved
Gastrointestinal disordersPancreatic failure✓ Approved

相关研究文献

PubMedCarbohydrate polymers2026-06-13

The rheological behavior, particle properties and supramolecular structure of low acyl gellan gum fluid gels: impact of the calcium concentration before fluid gel formation.

D'Oria Gabriele G, Zhu Yanshen Y, Limbach Hans Joerg HJ, Hartmann Christoph C et al.

Fluid gels are jammed microgel suspensions obtained by shearing a gelling hydrocolloid during its sol-gel transition. This study focused on calcium-induced low acyl gellan gum (LAGG) fluid gels and investigated the impact of calcium concentration before fluid gel formation on the resulting rheological behavior, fluid gel particle properties, and supramolecular structure. The elasticity and yield stress of fluid gels and quiescently cooled gels reached a maximum when the calcium concentration was increased from 0.78 to (approx.) 30 mmol/kg. Small angle X-ray scattering (SAXS) of fluid gels revealed a progressive increase in gel network connectivity up to the calcium concentration where the peak in rheological properties was observed followed by a less interconnected network at calcium concentrations above the peak. Furthermore, rheological measurements supplemented with free calcium and zeta-potential measurements, support that the decrease after the peak in rheological response is due to the combination of fluid gel particle softening with a decrease in surface charge. The results of this study enable to establish clearer links between rheological behavior, particle properties and supramolecular structure of calcium-induced LAGG fluid gels. This work enables a more effective design of fluid gel properties for different applications from food to pharma and biomaterials.

PMID 42285681
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PubMedAAPS PharmSciTech2026-06-13

Twin-Screw Melt Granulation with Mannitol: High-Drug-Loaded Immediate-Release Tablets of Caffeine.

Buczkowska Elzbieta Maria EM, Kukuls Kirils K, Horváth Zoltán Márk ZM, Frolova Alīna Jaroslava AJ et al.

High drug-loaded immediate-release formulations can be produced using a solvent-free and continuous melt-granulation method with a twin-screw extruder. Known and widely used high-molecular-weight and hydrophobic melt-binders result in weak tablets and negatively influence the disintegration and dissolution of tablets. Thus, this work aimed to probe mannitol as a melt-binder at a concentration of 30 wt.% and to investigate the effect of twin-screw melt granulation processing temperature and screw speed on the preparation of high drug-loaded immediate-release caffeine tablets with superior mechanical properties. A two-level design of experiment with three center points was used for the screening of the effect of barrel temperature and screw speed on granules and tablets properties. Model drug caffeine was mixed with mannitol (Parteck® M100), while a Pharma 11 extruder with helix feed screw elements and without a nozzle was used for twin-screw melt granulation. Processing conditions were found to significantly influence the solid state of ingredients and the quality of granules. Mannitol, as a melt-binder at a concentration of 30 wt.% at given processing conditions, was proven as an efficient melt-binder for high drug-loaded immediate-release tablets with superior mechanical properties.

PMID 42286306
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PubMedOncogenesis2026-06-13

Testican-1 activates Wnt/β-Catenin signaling to drive colorectal cancer progression.

Li Yi Y, Huang Chuying C, Zhang Chu C, Feng Lian L et al.

Colorectal cancer (CRC) ranks second in cancer-related mortality worldwide. Its clinical intractability and chemoresistance pose significant challenges, often driven by cancer stem cells (CSCs). Wnt/β-catenin signaling is a lynchpin of CSC self-renewal, but targetable upstream drivers remain elusive. Using bioinformatics, we identified the proteoglycan SPOCK1 (encoding the protein Testican-1) as a Wnt-associated marker. High SPOCK1 gene expression predicted poor patient prognosis and reduced progression-free survival following first-line chemotherapy. In vitro assays demonstrated that Testican-1 levels modulated Wnt/β-catenin activity. Testican-1 downregulation inhibited β-catenin nuclear translocation and TCF/LEF-mediated transcription, leading to concurrent suppression of CRC proliferation and spheroid-forming potential. Conversely, Testican-1 overexpression promoted β-catenin nuclear translocation and TCF/LEF-mediated transcription, which enhanced CRC malignant properties. This Testican-1-driven pro-tumorigenic effect was reversed by the β-catenin/TCF/LEF inhibitor iCRT3, demonstrating Testican-1's dependence on Wnt transcriptional activation. We validated this functional role in vivo using a Testican-1-overexpressing xenograft model and ex vivo using patient-derived organoids (PDOs), both confirming increased growth and β-catenin nuclear localization. Furthermore, data-independent acquisition (DIA) mass spectrometry of Testican-1-overexpressing tumors showed enrichment in Wnt/β-catenin and pro-tumorigenic pathways, including c-Myc and oxidative phosphorylation. Notably, Testican-1 expression was associated with remodeling of the tumor microenvironment, characterized by desmoplastic features. In summary, our findings establish a novel Testican-1/Wnt/β-catenin axis driving CRC tumorigenesis and progression, positioning it as a promising therapeutic target to overcome Wnt-mediated progression and resistance.

PMID 42285945
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PubMedNutrition & diabetes2026-06-13

The impact of 1-hour plasma glucose on the metabolic characteristics and pregnancy outcomes in polycystic ovary syndrome.

Huang Xiu X, Lu Nan N, Yu Hui H, Yang Fan F et al.

To investigate the impact of 1-hour plasma glucose (1 h-PG) on the metabolic characteristics and pregnancy outcomes in polycystic ovary syndrome (PCOS). This multicenter study analyzed 970 PCOS patients (2019-2025), including 289 undergoing assisted reproductive technology (198 successful deliveries). Participants were stratified by glucose tolerance: Group 1 (normal: fasting PG [FPG] ≤ 6.1, 1 h-PG < 8.6, 2-hour PG [2 h-PG] <7.8 mmol/L); Group 2 (isolated 1 h-prediabetes: 8.6 ≤ 1 h-PG < 11.6, FPG ≤ 6.1, 2 h-PG < 7.8 mmol/L); Group 3 (traditional 2 h-prediabetes: 7.8 ≤ 2 h-PG ≤ 11.1, FPG ≤ 6.1 mmol/L). Data included anthropometrics, metabolic biomarkers, sex hormones, and pregnancy outcomes were compared across three groups. PCOS with isolated 1 h-prediabetes (Group 2) had a more unfavorable metabolic profile with regard to metabolic traits, but were not significantly different from those of the traditional 2 h-prediabetes (Group 3). The adjusted odds ratios (ORs) for hypertension, hyperlipidemia, metabolic syndrome (MetS), and hyperuricemia in PCOS with Group 2 were 1.451 (1.013-2.079, P = 0.042), 1.706 (1.188-2.450, P = 0.004), 2.957 (1.755-4.981, P < 0.001), 1.890 (1.327-2.692, P < 0.001), respectively. For pregnancy outcomes, PCOS in Group 2 were more likely to progress to gestational diabetes mellitus (GDM) than those of Group 1, which was similarly observed in Group 3. The adjusted OR for GDM in the Group 2 was 4.065 (1.530-10.800, P = 0.005). Our study demonstrated that similar to 2 h-PG, elevated 1 h-PG was associated with different metabolic disorders and GDM. Therefore, 1 h-PG may serve as an additional marker of adverse metabolic status in women with PCOS.

PMID 42285965
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PubMedGeneral and comparative endocrinology2026-06-13

Nucleobindin-derived peptides and stress regulation in vertebrates.

Sethi Paalki P, Nasri Atefeh A, Unniappan Suraj S

Stress response entails a complex array of interactions between the neuroendocrine system and physiological and behavioral effects. When a sensory stimulus is perceived as stressful, the brain triggers a response controlled by two key neuroendocrine systems: the sympathetic pathways for the "fight or flight" response, and the hypothalamus-pituitary-adrenal (HPA) axis, for a long-term stress response. Growing evidence suggests that nucleobindin (Nucb)-derived peptides nesfatin-1 and nesfatin-1-like peptide (NLP), two anorexigens and metabolic regulators, are also involved in stress regulation. Nesfatin-1 stimulates corticotropin-releasing hormone (CRH) in the hypothalamus to induce stress and satiety. Nesfatin-1 and NLP activate the stress axis, stimulating adrenocorticotropic hormone (ACTH) synthesis and modulating cortisol synthesis. Nesfatin-1 elicits stress behavior, such as anxiety and depression. Nesfatin-1 and NLP regulate both stress and metabolism, suggesting their role in interlinking these processes. This review discusses the involvement of nesfatin-1 and NLP in stress-related pathways in vertebrates, their mechanism of action, as well as existing knowledge gaps that warrant further research.

PMID 42285421
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PubMedInternational immunopharmacology2026-06-13

Galectin-1 exacerbates hepatic steatosis by impairing autophagy via interaction with FIP200.

Zheng Lujuan L, Xia Jing J, Ge Pengyu P, Sheng Jiaxing J et al.

The pathogenesis of non-alcoholic fatty liver disease (NAFLD) remains incompletely understood, particularly the regulatory mechanisms linking autophagy dysregulation to disease progression. While impaired hepatic autophagy is known to contribute to NAFLD, the upstream factors that suppress autophagic flux under metabolic stress are not well defined. In this study, we demonstrate that galectin-1 (Gal-1) acts as a key mediator of hepatic steatosis and metabolic dysfunction by directly inhibiting autophagy. Surprisingly, overexpression of Gal-1 in mice is sufficient to trigger a series of pathological features similar to those of NAFLD, including hepatic steatosis, dyslipidemia, and insulin resistance, even in the absence of dietary challenges. Proteomic profiling revealed that Gal-1 induces a pronounced blockade of autophagic flux, evidenced by p62 accumulation and impaired LC3-II conversion. Mechanistically, Gal-1 binds the core autophagy scaffold protein FIP200, disrupting ULK complex assembly and further suppressing FIP200 expression at both transcriptional and post-translational levels. Structural mapping and binding studies identified a specific bipartite interaction interface involving Gal-1 residues TYR120/PHE134 and the claw domain of FIP200, with a binding affinity (Kd = 113.1 μM) critical for its autophagy-inhibitory function. Crucially, point mutations disrupting this interaction abolished Gal-1-mediated autophagy suppression and insulin resistance in cellular models. Our results uncover the Gal-1-FIP200 axis as a previously unrecognized regulatory node in NAFLD pathogenesis, offering a promising target for therapeutic intervention in metabolic liver disease.

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