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OLipHEX delivery system

✓ Approved

PR Pharmaceuticals · therapeutic agent

What is OLipHEX delivery system?

OLipHEX delivery system is a therapeutic agent developed by PR Pharmaceuticals. It is approved for therapeutic indications via oral (po).

Drug Profile

CompanyPR Pharmaceuticals
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, PR Pharmaceuticals

Therapeutic Indications

OLipHEX delivery system is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Surgical and medical proceduresOral appliance application✓ Approved

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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-15

Development of Versatile Nanoparticle System for Efficient Drug Delivery into Pulmonary Endothelium.

Mohammed Afzaal N AN, Deng Zicheng Z, Misra Arnab A, Orzabal Marcus M et al.

Drug delivery precisely to the pulmonary vasculature represents a formidable challenge. Pediatric Acute Respiratory Distress Syndrome (PARDS) is an urgent public health concern accounting for high mortality and long-term morbidity due to severe damage to lung endothelial cells (ECs). Advanced target-specific therapeutic interventions to protect lung vasculature in PARDS are in dire need. FOXF1 protein is a critical mediator of lung angiogenesis and vascular repair after injury. However, whether FOXF1 is a useful pharmacological target for PARDS is unknown. Herein, we developed a universal nanoparticle-based Lung Endothelial Drug Delivery (LEDD) system to deliver hydrophobic small-molecule compounds specifically to lung ECs but not to other cells or organs. Based on single-cell RNA sequencing, FOXF1 expression was decreased in lung ECs in the mouse PARDS model. We used LEDD nanoparticles to restore FOXF1 by delivering a novel FOXF1-activating compound, TanFe[F], which prevents FOXF1 protein degradation. LEDD-TanFe[F] treatment increased FOXF1 protein and its activity in lung ECs in vitro and in vivo. LEDD-TanFe[F] treatment was non-toxic, well-tolerated, and improved mice survival in the PARDS model. LEDD-TanFe[F] reduced endothelial permeability, improved vascular repair, and alveolarization in injured neonatal lungs. LEDD-supported drug delivery precisely to lung ECs is a promising therapeutic approach in PARDS.

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PubMedDrug delivery and translational research2026-10-15

In vitro, ex vivo and in vivo evaluation of polyelectrolyte nanogels for mucosal vaccines.

Bonaccorso Angela A, Corteggio Annunziata A, D'Apice Luciana L, Cardamone Antonio A et al.

Nasal administration is investigated as an effective mucosal site suitable for non-invasive vaccine delivery and able to elicit both systemic and mucosal immunity. Delivery of proteins across the epithelial barrier is a key point to induce an immune response. In this framework, nanogels are properly designed to present the delivered antigen to the immune system, promoting their targeting to specific immune populations. Nanogels for nasal administration based on dextran sulfate and ϵ-poly-L-lysine have been prepared by polyelectrolyte complexation. To unlock the potential of mucosal vaccination, we evaluated nanogel for their ability to enhance antigen delivery across mucus barriers and promote immune activation. Using fluorescein-labelled ovalbumin as a model antigen, we investigated how nanogel governs antigen transport, cellular uptake, and presentation. Produced results showed that nanogel combines favourable physicochemical properties with mucoadhesive behaviour, enabling efficient interaction with the mucus layer. This translates into enhanced uptake and controlled intracellular trafficking in murine Bone Marrow-derived-Dendritic Cells, ultimately promoting effective antigen cross-presentation. Importantly, intranasal administration in vivo revealed prolonged antigen retention within the airway mucosa compared to the free antigen, indicating sustained local antigen availability. In addition, studies in human monocyte-derived macrophages provided preliminary information on the inflammatory response and intracellular fate of the nanogels in a human-relevant system. Together, these findings contribute to the preliminary preclinical characterization of the nanogel platform, while further studies are required to establish its immunogenicity and vaccine efficacy.

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Decoupling T cell cytotoxicity: a CCL21+ICAM1-based synthetic immune niche enhances tumor elimination by accelerating lytic hit delivery.

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Preserving T cell cytotoxic function during ex vivo expansion remains a major challenge for adoptive cancer immunotherapy. A synthetic immune niche (SIN) composed of immobilized CCL21 and ICAM1 was shown to improve T cell expansion while preserving cytotoxicity; however, it remains unclear which specific step of the T cell killing process is enhanced by the SIN stimulation. Here, we combined advanced imaging based on time-lapse microscopy with a mean-field model to analyze the distinct stages in killing of B16 melanoma cells by CD8[Formula: see text] T cells. This framework enabled us to resolve the tumor cell killing process into discrete steps throughout target cell engagement with SIN-treated T cells and lytic hit delivery. We found that tumor cell death is best explained by a multi-hit process, requiring approximately four discrete hits to trigger cell death. Model-based analysis identified a significant increase in the lytic hit-delivery rate, [Formula: see text], as the main kinetic change associated with the enhanced cytotoxicity of SIN-treated T cells. The target encounter rate, [Formula: see text], could not be reliably compared between conditions because it was practically non-identifiable in the untreated dataset. Global sensitivity analysis further showed that increasing lytic hit delivery has a stronger effect on tumour control than increasing target encounter rates. These findings fundamentally reorient our understanding of optimized T cell manufacturing, suggesting that the lytic execution step may be the primary rate-limiting bottleneck in this in-vitro system, and that engineering strategies targeting granule polarization or discharge warrant prioritization alongside affinity-enhancement approaches.

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PubMedReviews on recent clinical trials2026-10-15

Genital Tuberculosis (GTB): Insights into Diagnosis, Treatment, Clinical Trials and Patents-A Comprehensive Review.

Singh Anuradha A, Dutta Prottay P, Muztaba Mohammad M, Sahoo Swagatam S et al.

Genital Tuberculosis (GTB) represents a frequently unrecognized type of extrapulmonary Tuberculosis (TB) that affects the female reproductive system. The condition results in infertility, menstrual cycle disturbances, and pelvic pain. The condition is difficult to detect at an early stage because its mild symptoms can manifest in different body parts. Therefore, medical professionals require better methods for diagnosing and treating patients. This review aims to provide a comprehensive overview of the epidemiology, pathogenesis, clinical manifestations, diagnostic approaches, therapeutic strategies, and current advancements in the management of GTB. The study presents information on New Drug Delivery systems (NDDs), current clinical trials, and new patents to guide future research. A literature-based narrative review was conducted, focusing on peer-reviewed articles, clinical studies, patents, and recent advances in diagnostics and therapeutics of GTB. The study focused on three main areas: anatomical site-specific manifestations; laboratory instruments and drug medications. The fallopian tubes are the most commonly affected site (90-100%), followed by the endometrium (50-60%), ovaries (20-30%), cervix (5-10%), while involvement of the vagina and vulva is rare (<1%). The diagnosis of GTB becomes problematic because both its visible and hidden symptoms start to appear. The development of effective detection methods depends on both traditional diagnostic methods and modern molecular methods, which include specialized laboratory equipment, imaging techniques, and histopathology. Current clinical trials and new patent approvals demonstrate the development of new methods for diagnosing and treating GTB, including improved therapeutic approaches and drug delivery systems. GTB presents both diagnostic and treatment difficulties because patients show different symptoms that can remain hidden. The combination of methods for diagnosing and treating GTB, through improved therapeutic approaches and drug-delivery systems, will enhance detection, treatment outcomes, and the ability to maintain fertility. The research should investigate personalized medicine approaches, molecular diagnostic technologies, and new therapeutic delivery systems to address the existing clinical needs in GTB treatment.

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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-15

Product-Reshaped Gas-Phase Hydrodynamics Govern CO2 Electrolysis in Gas Diffusion Electrodes.

Alyahya Abdullah A AA, Tovar-Oliva Mayra S MS, Malimusi Blessings G BG, Murcia-López Sebastián S et al.

High-rate CO 2 electrolysis is commonly assessed using current density, single-pass conversion and Faradaic efficiency, but these global metrics do not indicate whether the local reaction environment required for selective multicarbon formation is preserved during scale-up. Using an experimentally validated, flow-direction-resolved continuum model of a Cu-based gas-diffusion-electrode (GDE) flow-cell system, we demonstrate that gas-fed CO 2 electrolysers behave as reacting-flow electrochemical reactors in which electrochemical conversion transforms the gas phase in the cathode compartment and makes it part of the reactor response. As cathode potential becomes more negative, CO 2 consumption, CO formation and consumption, and gaseous product evolution progressively dilute the CO 2 -rich reacting gas phase, altering gas composition, density and velocity and feeding back into reactant delivery and intermediate availability. This reaction-induced hydrodynamic response creates an operating window favoring ethylene formation and reveals a conservation-driven feedback that becomes unavoidable during scale-up: as electrode length, conversion and gaseous product formation increase, extended electrodes must preserve the spatial overlap between CO 2 delivery, CO generation, controlled CO consumption and limited dilution of the reacting gas phase.

PMID 42875864
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Pathological mechanisms of long non-coding RNA FOXD2-AS1 promoting osteosarcoma mediated by the COI-1/OCN/Runx-2 signaling pathway.

Ren Zhipeng Z, Deng Liandong L, Sun Jie J, Kang Yuxiang Y et al.

Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents. Despite three decades of research efforts, no significant improvement in patient survival rates has been achieved, highlighting the urgent need for in-depth investigation into its pathogenesis to develop novel therapeutic strategies and more effective drugs. FOXD2-AS1, a long non-coding RNA, has been implicated in the prognosis and survival of various cancers, but its role in OS remains underexplored. This study therefore aimed to investigate the functional involvement of FOXD2-AS1 in OS progression and to evaluate a biocompatible delivery system for its in vitro and in vivo application. We synthesized mPEG-PDPA hydrogel via free radical polymerization of 2-(diisopropylamino)ethyl methacrylate (PDA) and polyethylene glycol monomethyl ether acrylate (mPEG-AC), and employed this hydrogel as a delivery vehicle for FOXD2-AS1. The biocompatibility and safety of the empty hydrogel were first validated through both in vitro cell assays and in vivo animal experiments. To explore the mechanistic actions of FOXD2-AS1, we performed real-time quantitative PCR and Western blot analyses, and conducted transcriptome profiling to identify downstream pathways and associated genes. Our results demonstrated that the mPEG-PDPA hydrogel itself was non-toxic and reliable as a delivery vehicle. Functionally, FOXD2-AS1 promoted alkaline phosphatase (ALP) release and exacerbated the inflammatory response, thereby accelerating the development and deterioration of OS. Mechanistically, FOXD2-AS1 activated the F-box protein Coronatine Insensitive 1 homolog (COI-1)/OCN/Runx-2 signaling pathway, as confirmed by qPCR and Western blot. Transcriptome analysis further revealed that this process involved changes in cell migration, apoptosis, and cell cycle regulation, with CPS1-IT1, ANKRD10-IT1, TBC1D3P1-DHX40P1, and RGS5 identified as key associated genes. Collectively, our findings provide new insights into the pathological mechanisms of OS and offer valuable data support for future therapeutic strategy development.

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