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pancrelipase (Ultrase MT20 / Ultrase MT / Ultresa)

✓ Approved

Adare Pharma Solutions · PNLIP

What is pancrelipase?

pancrelipase is a therapeutic agent developed by Adare Pharma Solutions. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesUltrase MT20, Ultrase MT, Ultresa
CompanyAdare Pharma Solutions
Molecular TargetPNLIP
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Adare Pharma Solutions

Mechanism of Action

Molecular Targets

pancrelipase acts on 1 molecular target:

PNLIPpancreatic lipase (PL, PNLIPD)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

pancrelipase is developed for 3 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
InvestigationsFaecal fat increased✓ Approved
Gastrointestinal disordersSteatorrhoea✓ Approved
Gastrointestinal disordersPancreatic failure✓ Approved

Related Research Articles

PubMedJournal of agricultural and food chemistry2026-11-11

Structural Characterization of LDP-1, a Polysaccharide from Lyophyllum decastes, and Its Protective Effects against PEDV-Induced Intestinal Inflammation In Vitro and In Vivo.

Zhao Wen W, Wei Yuheng Y, Lin Changhua C, Zhao Shuo S et al.

Porcine epidemic diarrhea virus (PEDV) infection causes severe intestinal inflammation and barrier injury in piglets. In this study, a purified polysaccharide fraction, Lyophyllum decastes polysaccharide-1 (LDP-1), was isolated and structurally characterized, and its protective effects against PEDV-induced intestinal injury were evaluated in IPEC-J2 cells and piglets. LDP-1 predominantly comprised glucose and exhibited a peak molecular weight of 30.56 kDa, with an α-(1→4)-glucan backbone. In vitro, LDP-1, particularly under pretreatment and whole-process treatment, attenuated PEDV-induced inflammatory cytokine expression. In vivo, LDP-1 pretreatment reduced diarrhea, alleviated intestinal pathological injury, and partially restored villus-crypt morphology. LDP-1 also decreased intestinal interleukin-6 (IL-6), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) expression and restored zonula occludens-1 (ZO-1), Claudin-1, and Occludin expression. These findings indicate that LDP-1 protects against PEDV-induced intestinal inflammation and barrier injury and may serve as a potential natural protective agent.

PMID 43012683
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PubMedJournal of medical primatology2026-11-11

Antibody Prevalence and Immune Profiles of Simian T-Lymphotropic Virus Type 1 in Chinese Laboratory Macaques.

Min Fangui F, Wang Jing J, Liu Yongjie Y, Zhang Lan L et al.

Simian T-lymphotropic virus type 1 (STLV-1) shares a high level of genetic homology with that of human (HTLV-1) and naturally infects a large variety of old world non-human primate species. However, the prevalence of STLV-1 in Chinese laboratory macaques is still unknown. A serological survey of STLV-1 in 970 Chinese laboratory macaques from six regions was conducted, and the clinical immune responses in 24 cynomolgus macaques with natural STLV-1 infection were profiled. The antibody prevalence for STLV-1 in regions 1-6 was 4.5%, 6.5%, 5.0%, 8.5%, 14.5%, and 8.6%, respectively. A one-way ANOVA revealed significant differences in the OD405 nm values between the groups (p = 0.0085). Furthermore, the prevalence in region 5 was significantly higher than that in regions 1, 2, and 3 (χ2, p < 0.05). Both the OD405 nm values and prevalence (%) in rhesus macaques were significantly higher than those in cynomolgus macaques. Elevated leukocyte counts and cytokine levels were observed in natural infections; however, the Th1/Th2 cytokine ratio showed no significant difference between STLV-1 infected animals and healthy controls. Survey results indicated that regional differences and animal husbandry levels might affect the infection rates of STLV-1. The study also demonstrated that most STLV-1-infected macaques maintain a long-term asymptomatic infection with a balanced Th1/Th2 response.

PMID 43012132
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PubMedBMC plant biology2026-11-11

One variation, two regulatory modes? Novel insights into the transcriptional regulation of 1-FEH isoforms in chicory under abiotic stress.

Zhong Jiaxin J, Walter Cornelia C, Stefanic Gracia G, Harms Karsten K et al.

Chicory taproots are a major source of industrially extracted inulin. However, low temperatures at the end of the growing season cause significant inulin degradation. Inulin loss has been attributed to fructan 1-exohydrolase (1-FEH) activity, which is mediated by three isoforms, 1-FEH1, 1-FEH2a and 1-FEH2b, respectively. Previous breeding studies have indicated a prominent role for 1-FEH2b, while the relative contributions of different 1-FEH isoforms have not yet been clearly defined. We demonstrate that promoters of 1-FEH1 and 1-FEH2b (p1-FEH1, p1-FEH2b) are differentially activated by cold-inducible transcription factors CiNAC5 and CiDREB2, respectively. Furthermore, differential responses were observed for promoters of the closely related genes 1-FEH2a and 1-FEH2b, caused by a single-base variation in their DRE element core motif: While in p1-FEH2b the core motif GTCG mediates effective binding to and activation by CiDREB2, the respective sequence in p1-FEH2a (TTCG) renders this promoter insensitive to CiDREB2. Furthermore, we observed a strong co-activation of p1-FEH2b by CiDREB2B and CiMYB5, corroborated by direct protein-protein interaction of these transcription factors. Remarkably, all three 1-FEH genes are also activated by high temperatures and drought, i.e., climate change-related abiotic stress factors. The distinct expression patterns of 1-FEH1, 1-FEH2a, and 1-FEH2b under cold treatment suggest that these isoforms have specific roles in responding to cold stress. However, these genes are also likely to be involved in chicory's response to climate change-related abiotic stress factors such as high temperatures and drought. The differential regulation of their corresponding promoters reveals distinct signaling pathways. In summary, our observations shed light on the role of inulin metabolism in chicory's response to abiotic stress and identify potential targets for improving chicory inulin quality via targeted promoter editing.

PMID 43009786
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PubMedBMC infectious diseases2026-11-11

Association between GLP-1 receptor agonist use and risk of pneumonia and pyothorax in type 2 diabetes: a retrospective cohort study.

Tai Li-Hsiu LH, Tsai Ping-Kun PK, Wang Yu-Hsun YH, Yeh Chao-Bin CB et al.

To assess the association between Glucagon-like peptide-1 receptor agonist (GLP-1 RA) use and the incidence of pneumonia and pyothorax in patients with Type 2 diabetes mellitus (T2DM). T2DM is associated with an increased risk of pneumonia and its complications, including pyothorax. GLP-1 RAs, a class of antidiabetic medications, have demonstrated anti-inflammatory and cardiometabolic benefits, but their influence on infectious complications remains underexplored. This retrospective cohort study was conducted using data from the TriNetX U.S. collaborative network, which comprises electronic health records of over 116 million patients. Adults aged ≥ 20 years with a new diagnosis of type 2 diabetes mellitus (T2DM) between 2016 and 2023 were identified. Patients were divided into two groups based on exposure to glucagon-like peptide-1 receptor agonists (GLP-1 RAs) versus non-GLP-1 RA treatments. After applying exclusion criteria and performing 1:1 propensity score matching for demographics, comorbidities, medications, and relevant laboratory values, a total of 181,634 patients were included in the matched cohorts. The primary outcome was the incidence of pneumonia (ICD-10-CM codes J12-J18) and pyothorax (ICD-10-CM code J86). The incidence of pneumonia and pyothorax was significantly lower in the GLP-1 RA group (15.20%) compared to the non-GLP-1 RA group (18.54%), with a hazard ratio (HR) of 0.76 (95% CI: 0.74-0.78). GLP-1 RA use was also associated with reduced risk of pyothorax (HR = 0.58, 95% CI: 0.46-0.73). These protective effects were consistent across subgroups stratified by age, sex, race, and BMI, although not statistically significant among Asian and African American populations, likely due to limited sample size. GLP-1 RA therapy in T2DM patients is associated with a significantly lower risk of pneumonia and pyothorax, potentially mediated through anti-inflammatory and metabolic benefits. These findings support the broader role of GLP-1 RAs in mitigating infection-related complications in diabetes care. Not applicable.

PMID 43009800
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PubMedAesthetic plastic surgery2026-11-11

ICAM-1 Mediates the Immunosuppressive Activity of Adipose-Derived Stem Cells in the Inflammatory Environment.

Cao Jiankun J, Wang Chuan C, Yang Zhigang Z, Chen Hui H

Adipose-derived mesenchymal stem cells have gained attention in plastic and reconstructive surgery because they are efficient immunoregulators and easily accessible with minimal invasion. However, the mechanism of their immunoregulatory role in the inflammatory environment is unclear. Adipose-derived stem cells (ASCs) and peripheral blood mononuclear cells (PBMCs) were co-cultured to confirm the immunosuppressive activity of ASCs. The effects of inflammatory cytokines on the expression of vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1) in ASCs were evaluated using flow cytometry. Nuclear factor-κB (NF-κB) and molecular target of rapamycin (mTOR) signaling inhibitors were used to evaluate the mechanism of tumor necrosis factor alpha (TNF-α) stimulated upregulation of ICAM-1 in ASCs. To evaluate the effect of ICAM-1 knockdown on the immunoregulatory capacity of ASCs, PBMCs were labeled with carboxyfluorescein succinimidyl ester (CFSE), and their proliferation was analyzed using flow cytometry. ASCs inhibited PBMC proliferation. ICAM-1, and not VCAM-1, responded to pro-inflammatory cytokines and was upregulated by TNF-α in a concentration- and time-dependent manner; the NF-κB pathway inhibitor specifically blocked this increase in ICAM-1 expression. Knocking down ICAM-1 attenuated the immunosuppressive effects of ASCs on PBMC proliferation. ICAM-1, and not VCAM-1, is an inflammation sensor on ASCs and plays a key role in the immunoregulatory potential of ASCs. Pro-inflammatory TNF-α significantly increases ICAM-1 expression on ASCs in a concentration- and time-dependent manner, which is mediated by the NF-κB signaling pathway. These data may provide a theoretical basis for the clinical administration of ASCs in inflammation-related diseases in plastic and reconstructive surgery. This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

PMID 43009551
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PubMedPediatric critical care medicine : a journal of the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies2026-11-11

Postoperative Infection Mediates and Modifies the Effect of Risk Adjustment for Congenital Heart Surgery-1 Category on Hospital Stay in Pediatric Cardiac Surgery: A Retrospective Cohort Study.

Huang Jihong J, Gao Jiawei J, Shang Wenyuan W, Chen Sun S et al.

To investigate whether postoperative infection mediates and/or modifies the effect of surgical complexity, as defined by the Risk Adjustment for Congenital Heart Surgery (RACHS-1) category, on hospital length of stay (LOS) in pediatric cardiac surgery patients. Retrospective cohort study. Tertiary pediatric cardiac center at Xinhua Hospital, Shanghai Jiao Tong University. A total of 1244 children who underwent congenital heart surgery between October 2020 and July 2024. None. Multivariable regression and causal-mediation analyses were performed to estimate the direct and infection-mediated effects of surgical complexity on LOS. Higher-RACHS-1 categories and postoperative infection were independently associated with prolonged LOS (all p < 0.001). In negative binomial mediation analysis, infection mediated 17.4% of the total RACHS-LOS association for RACHS-1 category greater than or equal to 5 vs. 1, corresponding to an infection-mediated increase of 3.87 expected LOS days (95% CI, 1.70-6.42). Infection also modified the association between surgical complexity and LOS, with infection-associated excess LOS increasing to +16.73 days in RACHS-1 category greater than or equal to 5 vs. 1. Mediation was strongest among infants less than or equal to 1 year (28% for RACHS-1 category 3 vs. 1). Postoperative infection both mediates and amplifies the impact of surgical complexity on hospital LOS, particularly in high-risk infants. Targeted infection-prevention strategies are essential to reduce postoperative morbidity in this population.

PMID 43012614
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