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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

PubMedExperimental dermatology2026-07-25

Integrated Proteogenomics and Single-Cell Transcriptomics Prioritize Putative Protective Plasma Proteins for Hidradenitis Suppurativa.

Cheng Yuzhe Y, Ma Jingyi J, Niu Jun J

Translating hidradenitis suppurativa (HS) genetic susceptibility into actionable targets remains challenging, as most genome-wide association study loci lie in non-coding regions and tissue-level transcriptomics cannot easily distinguish causal drivers from secondary inflammation. In this study, we aimed to prioritize plasma proteins whose genetically predicted levels are causally associated with HS risk and to localize them within human skin at single-cell resolution. We performed two-sample Mendelian randomization (MR) using cis-pQTL instruments for 2923 plasma proteins from the UK Biobank Pharma Proteomics Project against HS summary statistics from FinnGen R12. Following multiple-testing correction and Bayesian colocalization with a prior-sensitivity grid, the intersection of false-discovery rate (FDR)-significant MR with colocalization evidence (PP.H4 ≥ 0.5) yielded three putative protective candidates: TNFRSF6B (OR = 0.748, 95% CI 0.666-0.840; PP.H4 = 0.648), FCRL2 (OR = 0.896, 95% CI 0.819-0.979; PP.H4 = 0.550), and APOD (OR = 0.789, 95% CI 0.647-0.963; PP.H4 = 0.503). All sensitivity MR tests were concordant. Single-cell transcriptomic analysis localized FCRL2 and APOD to specific cell populations. FCRL2 was predominantly expressed in B cells and NK cells, while APOD showed multi-cellular expression across cornified keratinocytes, macrophages, and dendritic cells. Furthermore, TNFRSF6B was below the skin detection threshold, supporting its biological role as a circulating decoy receptor. Together, our integrated proteogenomic and single-cell approach prioritizes TNFRSF6B, FCRL2, and APOD as putative protective plasma proteins for HS, with TNFRSF6B emerging as the most genetically robust candidate for future translational follow-up.

PMID 42499219
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PubMedThe Journal of nutrition2026-07-25

Biological mechanisms underlying the cardiovascular effects of branched-chain amino acids: A proteome-wide Mendelian Randomization Study.

Zhang Junmeng J, van Dam Rob M RM, Zhao Jie V JV

Ischemic heart disease (IHD) is the leading cause of morbidity and mortality. Branched-chain amino acids (BCAAs) are associated with higher IHD risk, but the underlying biological pathways remain unclear. This study aims to explore these pathways using two-step proteome-wide Mendelian randomization. We examined the associations between genetic proxies for BCAAs and 2,922 proteins in the UK Biobank Pharma Proteomics Project (UKB-PPP), supplemented by a meta-analysis with data from deCODE to identify proteins associated with BCAAs. Then we tested their effects on IHD risk using CARDIoGRAMplusC4D (122,733 cases, 424,528 controls) and replicated in FinnGen (31,640 cases, 187,152 controls). We conducted sensitivity analyses using genetic instruments from deCODE. Proteins associated with IHD risk and, in a consistent direction, with genetically predicted BCAAs were considered potential mediators. Genetic proxies for BCAAs were associated with 40 proteins. Among these, six proteins showed consistent evidence of mediation, including complement component 1s (C1S), coagulation factor II (F2), granulin (GRN), proprotein convertase subtilisin/kexin type 9 (PCSK9), sex hormone-binding globulin (SHBG) and V-set and transmembrane domain-containing Protein 2 Like (VSTM2L). These proteins are involved in inflammation, coagulation, lipid metabolism and cellular stress response. All associations were robust across different analytical methods and replicated in independent datasets. Mediation analysis showed that these proteins accounted for 6.5% to 32.1% of the association between BCAAs and IHD risk. This study identified six proteins that potentially link BCAAs to IHD, implicating pathways related to inflammation, coagulation, lipid metabolism, and cellular stress responses. These findings provide novel mechanistic insights into the BCAA-IHD relationship and highlight potential protein targets for future prevention and intervention strategies.

PMID 42498029
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PubMedNature communications2026-07-25

JN.1-adapted vaccination is associated with readjustment of ancestral memory B cells toward neutralization within the JN.1 antigenic space.

Stankov Metodi V MV, Bruhn Matthias M, Hoffmann Markus M, Salam Abdus A et al.

The antigenic drift of SARS-CoV-2 toward the JN.1 lineage has prompted the development of variant-adapted COVID-19 booster vaccines. However, these boosters are thought to primarily recall pre-existing memory B cells (MBC), raising concerns about their ability to realign the immune response in highly pre-exposed populations. Here we analyze antibody and B cell responses in pre-exposed individuals (n = 42; median 4.5 prior COVID-19 vaccinations; 90% with at least one prior SARS-CoV-2 infection) following vaccination with a JN.1-adapted mRNA vaccine. Vaccination is associated with increased IgG binding and enhanced neutralization of JN.1 and related descendant variants. Longitudinal profiling of antigen-specific MBC shows that Wu01-only and Wu01/JN.1 cross-reactive cells remain dominant, while JN.1-only cells modestly increase by day 21. Single-cell RNA-sequencing of antigen-specific MBC in a representative sub-cohort (n = 7), combined with functional monoclonal antibody analyses, demonstrates that somatic hypermutation (SHM) drives intra-clonotype specialization toward improved JN.1 binding and neutralization. These findings indicate maturation of pre-existing, class-switched MBC rather than substantial de novo recruitment of naïve B cells. In conclusion, JN.1-adapted booster vaccination is associated with refinement of pre-existing MBC repertoires toward the JN.1 antigenic space and with enhanced neutralization of contemporary and antigenically proximate variants.

PMID 42498786
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PubMedNanoscale advances2026-07-25

Rice straw-derived activated carbon/ZnO nanocomposite as a high-performance electrode for asymmetric supercapacitors.

Raza Asif A, Mbs Pravin P, Rajendran Divya D, Sarwar Zartasha Z et al.

The synthesis of electrode materials from biomass waste has attracted considerable attention due to their low cost and high electrochemical performance in energy devices. Therefore, in this study, activated carbon was prepared from rice straw waste and composited with zinc oxide (ZnO) nanoparticles to enhance the electrochemical performance of an asymmetric supercapacitor. AC, ZnO, and AC-ZnO exhibit specific surface areas of 201, 255, and 578 m2 g-1, respectively, with average pore diameters of 1.37 nm, 1.73 nm, and 2.45 nm, respectively. The AC-ZnO composite exhibited a higher specific capacitance of 244 F g-1, compared with 206 F g-1 for ZnO and 137 F g-1 for AC at a current density of 0.5 A g-1. The charge-transfer resistance (R ct) values for AC, ZnO, and AC-ZnO were 0.050, 0.061, and 0.035 Ω, respectively. After 10 000 charge-discharge cycles, the corresponding capacitance retentions were 83.5%, 75.3%, and 89.9%, respectively. The AC-ZnO composite exhibits a hybrid capacitive behavior due to the electrical double-layer capacitor behavior of AC and the pseudocapacitive behavior of ZnO. The specific capacitance, energy density, and power density of the assembled device are 149 F g-1, 20.66 Wh kg-1, and 500 W kg-1, at 1 A g-1. Moreover, the assembled device exhibited 97% capacitance retention and 100% coulombic efficiency after 5000 charge-discharge cycles.

PMID 42499689
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PubMedBlood advances2026-07-25

Tenecteplase (TNK) and other TNK formulations lose PAI-1 resistance in their two-chain form: Comparison with alteplase.

Liu Zikou Z, Tippett Isabel I, McCutcheon Fiona M FM, Keragala Charithani B CB et al.

Alteplase is synthesized as a single-chain protease that requires plasmin-mediated conversion to its fully active two-chain form for maximal thrombolysis. Tenecteplase (TNK), an alteplase variant, is widely regarded as being more fibrin-selective and more resistant to plasminogen activator inhibitor-1 (PAI-1) than alteplase. However, the PAI-1 sensitivity of TNK after two-chain conversion, and that of newly available TNK formulations, has not been evaluated. Alteplase and four TNK formulations: Metalyse (Boehringer Ingelheim), Tenectase (Gennova, India), GenetPA (BioApower, China) and Mingfule (CSPC, China) were compared in their native state and after two-chain conversion. Proteolytic activity, PAI-1 resistance and binding were evaluated using amidolytic assay, fibrinolysis assays and Western blotting. Alteplase, but not Metalyse was converted into its two-chain form in plasma in a fibrinogen-dependent manner, resulting in off-target fibrinogenolysis. When directly reconstituted from the manufacturers vial (native form), TNK was ~4-fold more resistant to PAI-1 than alteplase; however, two-chain conversion significantly reduced PAI-1 resistance by ~40%, concomitant with increased PAI-1 binding. Native Metalyse contained ~3-fold more pre-existing two-chain species than the other TNK formulations, explaining its higher amidolytic activity. However, after two-chain conversion, all TNK formulations showed similar fibrinolytic activity albeit with substantially reduced PAI-1 resistance. Metalyse and all new TNK formulations display similar fibrinolytic activity in their fully active two-chain states, but this is associated with substantial loss of PAI-1 resistance, challenging the view that the fully active two-chain form of TNK maintains PAI-1 resistance during thrombolysis.

PMID 42498282
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PubMedIndian journal of clinical biochemistry : IJCB2026-07-25

Short-Chain Fatty Acids Ameliorates Lipid Profile, Oxidative Stress and Inflammation in Letrozole Induced Polycystic Ovary Syndrome Rat Model.

Acharya Ashwitha A, Shetty Prasanna Kumar PK, Sonkusare Shipra S, Padmanabha Ganeshkodi Roopashree R et al.

Polycystic ovary syndrome (PCOS) is one of the most common metabolic-reproductive disorders affecting reproductive-age women, causing an irregular menstrual cycle, hyperandrogenism, and polycystic ovarian morphology. Current therapies for PCOS focus on the management of symptoms. Short-chain fatty acids (SCFAs) play a significant role in PCOS by influencing the gut microbiota composition and metabolic pathways. The impact of short-chain fatty acids (SCFAs) on lipid profiles, inflammatory markers, and oxidative stress parameters in the PCOS model remains unclear. The present study aimed to elucidate the effect of SCFA on lipid profile, oxidative stress parameters, and inflammation in a high-fat diet-fed letrozole-induced PCOS model. 48 Female albino Wistar rats were randomised to 8 group (n = 6). The groups were treated with letrozole to induce PCOS and then treated with sodium acetate (SA), sodium propionate (SP), sodium butyrate (SB), and SCFA (3:1:1) mixture. This study observed a significant distortion in lipid profile, oxidative stress parameters and inflammatory markers. Our data showed, PCOS model showed elevated levels of triglycerides and very-low-density lipoprotein, which were significantly ameliorated when treated with SCFA (3:1:1), SA, SP, and SB. SP, SB, and SCFA (3:1:1) significantly lowered total cholesterol, while only SB and SCFA (3:1:1) significantly lowered low-density lipoprotein-cholesterol. Elevated high-density lipoprotein-cholesterol was observed in the SA, SB, and SCFA (3:1:1) treated group. The malondialdehyde level was lowered in the SCFA-treated groups, whereas the total antioxidant capacity, superoxide dismutase, and glutathione level was elevated. Our data showed a significant reduction in IL-6, IL-1β levels in the PCOS-induced group treated with SA, SP, SB, and SCFA (3:1:1). The findings of the present study suggest that short-chain fatty acids restructure dyslipidemia, oxidative stress and inflammation in a PCOS-induced model, highlighting their possible role as therapeutic dietary supplements in alleviating PCOS.

PMID 42500348
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