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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

PubMedYi chuan = Hereditas2026-07-17

The retrotransposon LINE-1: a double-edged sword in tumorigenesis.

Tian Lu L, Liu Qian Q, Cen Shan S, Li Xiao-Yu XY

Transposons, also known as jumping genes, are DNA sequences capable of relocating within or between chromosomes. Long interspersed element-1 (LINE-1), the only autonomously active retrotransposon in the human genome, plays a critical role in maintaining genomic stability through its dynamic regulation. Under normal physiological conditions, the host employs epigenetic and other mechanisms to maintain LINE-1 in a silenced state. However, when this precise regulatory control is disrupted, aberrant LINE-1 activation can lead to insertional mutations, resulting in genomic instability and the development of various genetic disorders and malignant tumors. Recent evidence has demonstrated elevated LINE-1 expression in multiple cancers, such as breast, esophageal, lung, and colorectal cancer, suggesting a close association between LINE-1 dysregulation and tumorigenesis. This review summarizes the multi-layered regulatory network governing LINE-1, encompassing epigenetic modifications, non-coding RNAs, and various host restriction factors. It also explores the molecular mechanisms underlying LINE-1 aberrant activation in the tumor microenvironment and outlines the diverse pathways through which LINE-1 influences tumor development, such as compromising genomic stability, triggering inflammation and immune responses, and participating in cellular immortalization. This review not only provides a theoretical foundation for utilizing LINE-1 as a molecular biomarker in cancer diagnosis but also offers new perspectives for developing novel anti-tumor therapeutic strategies based on LINE-1 regulation.

PMID 42464724
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PubMedJournal of the American Heart Association2026-07-17

Comparative Cardiovascular Outcomes of Tirzepatide and Glucagon-Like Peptide-1 Receptor Agonists in Patients With Type 2 Diabetes and Atherosclerotic Cardiovascular Disease.

Wu Jheng-Yan JY, Lee Keng-Wei KW, Kao Chia-Li CL, Hung Kuo-Chuan KC et al.

To evaluate the association between tirzepatide use and 1-year risk of major adverse cardiovascular events in patients with type 2 diabetes and atherosclerotic cardiovascular disease, compared with GLP-1 (glucagon-like peptide-1) receptor agonists. We conducted a retrospective, propensity score-matched cohort study using the TriNetX network. A total of 16 402 patients with type 2 diabetes and atherosclerotic cardiovascular disease initiating tirzepatide or GLP-1 receptor agonists between January 1, 2022, and March 31, 2025 were matched 1:1. The primary outcome was 1-year major adverse cardiovascular events; secondary outcomes included all-cause mortality, acute myocardial infarction, major adverse limb events, and tissue plasminogen activator use. Tirzepatide was associated with a lower risk of major adverse cardiovascular events (hazard ratio [HR], 0.75 [95% CI, 0.63-0.91]) and reduced risks of all-cause mortality (HR, 0.69 [95% CI, 0.53-0.90]), major adverse limb events (HR, 0.59 [95% CI, 0.39-0.88]), and acute myocardial infarction (HR, 0.70 [95% CI, 0.53-0.93]), compared with GLP-1 receptor agonists. Results were robust across subgroups and sensitivity analyses. Among patients with type 2 diabetes and atherosclerotic cardiovascular disease, tirzepatide was associated with a significantly reduced 1-year risk of major adverse cardiovascular events and other cardiovascular outcomes compared with GLP-1 receptor agonists. These findings support the cardiometabolic potential of tirzepatide, warranting further prospective validation.

PMID 42466510
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PubMedbioRxiv : the preprint server for biology2026-07-17

Proximity labeling at H3K9me3 reveals VRK-1 regulate global chromatin distribution in C. elegans.

Smith William W, Aksianiuk Valeryia V, Pfaendler Ramon R, Villaseñor Rodrigo R et al.

Heterochromatin marked by histone H3 lysine 9 di- or trimethylation (H3K9me2/3) underpins transcriptional silencing and nuclear organization, yet its full complement of associated proteins remains incompletely defined. Here, we apply ChromID proximity labelling with the mouse HP1? chromodomains to map the H3K9me3-proximal proteome in Caenorhabditis elegans, recovering known heterochromatin factors alongside previously uncharacterized candidates. We pursued one such candidate, the vaccinia-related kinase VRK-1, because of its established but poorly understood links to chromatin organization. Intriguingly, VRK-1 dynamically relocates from a broad nuclear distribution to the nuclear periphery upon azide or heat stress. Following these stresses, bulk chromatin exhibits similarly increased peripheral enrichment and apparent compaction, as assessed by radial fluorescence profiles. Although VRK-1 is not necessary for stress-induced chromatin reorganization, decompaction and repositioning of chromatin away from the nuclear envelope during recovery requires VRK-1. VRK-1 depletion leads to persistent perinuclear chromatin retention and compromises post-stress survival. Furthermore, loss of VRK-1 catalytic activity results in over-retention of chromatin at the nuclear periphery under normal growth conditions; this phenotype can be reversed by depletion of a key VRK-1 substrate at the nuclear envelope BAF-1. Our findings identify VRK-1 as a key regulator that controls the interaction of chromatin with the nuclear lamina through regulation of BAF-1.

PMID 42465445
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PubMedbioRxiv : the preprint server for biology2026-07-17

Dichloroacetate improves animal survival, growth, neuromuscular activity, mitochondrial stress and physiology, and elevated lactate in C. elegans pdha-1 and dld-1 RNAi models of pyruvate dehydrogenase complex deficiency (PDCD).

Remes Cristina C, Mathew Neal D ND, Miranda Victoria V, Haroon Suraiya S et al.

Pyruvate dehydrogenase complex (PDHc) deficiency (PDCD) is a primary mitochondrial disorder characterized by neurodevelopmental disability, altered intermediary metabolism and early mortality. Dichloroacetate (DCA), a pyruvate analogue, is a well-described PDHc activator that remains under clinical investigation for treatment of PDCD. Here, we studied the in vivo efficacy of a 5-point log concentration range of DCA on animal health and metabolism in C. elegans with feeding RNA interference (RNAi) expression knockdown of either PDHA-1 or DLD-1 homologues at graded degrees to model variable disease severity. These worm models recapitulate phenotypic features of PDCD observed in human patients, including reduced survival, delayed growth, locomotor impairment, and elevated lactate and/or pyruvate tissue levels. DCA treatment appeared well-tolerated, with no gross morphologic toxicity seen at doses up to 25 mM. Significantly improved health, survival, tissue lactate levels, and mitochondrial physiology were observed at 25 mM in pdha-1(RNAi) knockdown animals. DCA treatment in dld-1(RNAi) C. elegans models (undiluted, 1:20 dilution, and 1:100 dilution) showed significant therapeutic benefits on survival, neuromuscular function and metabolic phenotypes primarily in the moderate (1:20) and/or mild (1:100) dld-1(RNAi) deficiency strains, but not in full-dose dld-1(RNAi) . Importantly, linear growth, neuromuscular activity, and mitochondrial physiology were significantly improved with DCA treatment even in the most severe dld-1(RNAi) undiluted model. Overall, preclinical modeling provides objective evidence of DCA therapeutic efficacy in C. elegans expression knockdown strains for two well-conserved homologues of PDHA1 and DLD that represent distinct genetic etiologies of PDHc deficiency, with demonstrated beneficial effects on survival, healthspan, tissue lactate, and mitochondrial physiology. These data further confirm that DCA's therapeutic effect correlates with PDHc disease phenotype severity in dld-1(RNAi) animals. SYNOPSIS: Dichloroacetate (DCA) treatment demonstrated significant preclinical beneficial effect on survival, neuromuscular function, linear growth, tissue lactate, and mitochondrial metabolism in two C. elegans models with variable degrees of pyruvate dehydrogenase complex (PDHc) deficiency (PDCD), providing confirmatory evidence to support its therapeutic potential in human PDCD patients.

PMID 42465370
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PubMedJAMA health forum2026-07-17

Postshortage Compounded GLP-1 RA Market in 2 States With Potentially High Demand.

DiStefano Michael J MJ, Tilley Adeleine A, Paratane Deepika D, Gyimah Gyamfi Harry H et al.

Supply-side challenges combined with high costs and limited insurance coverage led to a robust market for compounded glucagon-like peptide-1 receptor agonists (GLP-1 RAs). However, assessment of this market since the end of the semaglutide and tirzepatide shortages is needed. To characterize available compounded GLP-1 RA products, describe aspects of patient care and monitoring, and identify source pharmacies of available compounded products. From August to October 2025, a cross-sectional secret shopper study was conducted of brick-and-mortar weight-loss clinics and medical spas advertising GLP-1 RAs for weight loss and offering compounded GLP-1 RAs. These businesses were identified in January 2025 using a web mapping application to perform location-based searches that were supplemented with a review of business websites and publicly available data regarding compounding facilities. The businesses were located in 2 states (West Virginia and Oklahoma) with potentially high demand for compounded GLP-1 RAs that were purposively selected based on obesity rate and insurance mix. Compounded GLP-1 RAs offered by weight-loss clinics and medical spas; aspects of patient care and monitoring; and characteristics of compounding suppliers, including facility type, licensing status, objectionable conditions noted by investigators, and disciplinary actions. A total of 75 weight-loss clinics and medical spas offering compounded GLP-1 RAs were identified and included in the analysis. Of these businesses, 7 (9.3%) reported offering oral compounded GLP-1 RA formulations and 42 (56.0%) reported offering compounded GLP-1 RA products combined with B vitamins. Twenty-three compounding facilities were identified as suppliers, 4 (of 21; 19.0%) of which were not licensed to perform sterile compounding. Since 2023, 1 facility (4.3%) had received multiple US Food and Drug Administration warning letters and 3 of 22 (13.6%) had been subject to state-level disciplinary action. Findings of this study show that, after the end of the semaglutide and tirzepatide shortages, compounding facilities have continued to manufacture GLP-1 RAs with added ingredients. Compounded GLP-1 RA sourcing is diverse but includes facilities without licenses to perform sterile compounding or that have been subject to recent disciplinary action, posing clinical and regulatory challenges.

PMID 42467450
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PubMedbioRxiv : the preprint server for biology2026-07-17

PSGL-1 blockade delays relapse to BRAF/MEK inhibition in cutaneous melanoma.

El Naggar O S OS, Ha B N BN, Rakoto M L ML, Cort L L et al.

Advanced BRAF-mutant cutaneous melanoma can be treated with targeted therapy when immune checkpoint inhibitors (ICIs) fail or are not a feasible option. Nevertheless, most patients do not achieve a durable response, highlighting the critical need for therapeutic partners that enhance the long-term efficacy of targeted therapy. Transcriptomic analysis of a BRAF-mutant melanoma model of acquired resistance identified P-selectin glycoprotein ligand-1 (PSGL-1) as a top-upregulated immune mediator upon resistance acquisition. PSGL-1 is a key regulator of CD8 + T cell exhaustion and differentiation, and its inhibition has been shown to enhance T cell function across multiple disease models. Based on these observations, we hypothesized that combined targeting of BRAF/MEK and PSGL-1 would improve anti-tumor responses. Here, we demonstrate that dual inhibition of BRAF/MEK and PSGL-1 elicits durable tumor control in a preclinical model of PD-1-refractory cutaneous melanoma. Single-cell RNA sequencing of the tumor microenvironment reveals robust reprogramming of intratumoral CD8 + T cells toward a less terminally differentiated, memory-like phenotype following combined BRAF/MEK and PSGL-1 targeting. Consistent with these findings, CD8 + T cells in the tumor-draining lymph nodes of PSGL-1 -/- mice exhibit enhanced functionality and a less differentiated state of exhaustion when compared with wild-type mice. To extend these observations to a translationally relevant setting, we further show that antibody-mediated blockade of PSGL-1, in combination with BRAF/MEK inhibition, yields superior anti-tumor activity compared with either monotherapy. Collectively, these findings identify PSGL-1 as a promising therapeutic target to enhance the durability of targeted therapy and provide a strong rationale for future clinical evaluation.

PMID 42465267
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