Drug Database
MA

mannitol (Aridol / Osmohale)

✓ Approved

Syntara · Small Molecule · Small Molecule

What is mannitol?

mannitol is a small molecule developed by Syntara. It is approved for therapeutic indications via inhaled.

Drug Profile

Brand NamesAridol, Osmohale
CompanySyntara
Drug ClassSmall Molecule
RouteInhaled
StatusApproved
Sources: ClinicalTrials.gov, Syntara

Therapeutic Indications

mannitol is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Respiratory, thoracic and mediastinal disordersRespiratory failure✓ Approved

Related Research Articles

PubMedGenes & diseases2026-09-20

ZO-2 blocks the localization of PGAM5 protein to the mitochondrial membrane and suppresses pancreatic cancer malignancy through metabolic reprogramming.

Yu Sen S, Ke Mingxin M, Ma Muyuan M, Jiang Tingting T et al.

Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related death with limited treatment options, and there is an urgent need to develop effective therapeutic strategies. The zonula occludens-2 (ZO-2) protein is a member of the tight junction protein family, and its function and underlying mechanisms of action in PDAC are unknown. Gene expression and its association with the clinicopathologic characteristics of patients with PDAC were analyzed using immunohistochemistry and bioinformatics and functionally validated by using in vitro and in vivo mouse models. Protein expression and protein regulation were measured by using gain- and loss-of-function assays and molecular biology methods. The expression level of ZO-2 decreased in PDAC and was highly correlated with aggressive pathological features and the prognosis of patients. Increased expression of ZO-2 inhibited the proliferation, migration and colony formation of PDAC cells in vitro and inhibited PDAC tumor growth and liver metastasis in vivo. Mechanistically, ZO-2 bound to the mitochondrial membrane protein phosphoglycerate mutase 5 (PGAM5) and trapped it in the cytosol. Reduced expression of ZO-2 caused increased mitochondrial localization of PGAM5, leading to activated mitochondrial function and increased intracellular reactive oxygen species and ATP levels, thereby promoting PDAC malignancy, whereas increased ZO-2 expression did the opposite. ZO-2 expression also correlated directly with immune cell infiltration and immune signaling in PDAC. Downregulation of ZO-2 caused increased localization of PGAM5 to the mitochondrial membrane and promoted PDAC malignancy through metabolic reprogramming. ZO-2 is associated with the PDAC immune microenvironment. The ZO-2-PGAM5 axis could serve as a potential therapeutic target in PDAC.

PMID 42763477
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PubMedInternational journal of general medicine2026-09-20

Clinical and Genetic Factors Associated with Multivessel Coronary Artery Disease: A Cross-Sectional Study of CYP2C19 Polymorphisms and Metabolic Comorbidities.

Cai Nan N, Li Youqian Y, Liu Jingfeng J, Hong Haifeng H et al.

Multi-vessel coronary artery disease (MVCD), defined as stenosis affecting ≥2 major coronary arteries, confers poor clinical outcomes in patients with coronary artery disease (CAD). Cytochrome P450 2C19 (CYP2C19) CYP2C19 participates in lipid metabolism and inflammatory regulation, which may be associated with individual variations in the severity of coronary artery lesions. This study aimed to explore the clinical and genetic factors associated with MVCD focusing on CYP2C19 polymorphisms and chronic metabolic diseases. This single‑center cross‑sectional study enrolled 4124 patients with angiographically confirmed CAD, who were divided into single‑vessel CAD (n=846) and MVCD (n=3278) groups. Baseline clinical data and CYP2C19 genotypes were collected. The chi-square test, Hardy-Weinberg equilibrium test, and logistic regression analyses were performed for statistical evaluation. Higher prevalences of hypertension, type 2 diabetes mellitus, and dyslipidemia were observed in MVCD patients. CYP2C19*2 (rs4244285, 681G>A) and *3 (rs4986893, 636G>A) allele frequencies were markedly elevated in the MVCD group. Logistic regression analysis confirmed that hypertension (odds ratio (OR)=1.485, 95% confidence interval (CI): 1.267‑1.740, p<0.001), T2DM (OR=2.441, 95% CI: 2.006‑2.970, p<0.001), dyslipidemia (OR=1.313, 95% CI: 1.097‑1.572, p=0.003), and CYP2C19 poor metabolizer (*2/*2, *2/*3 and *3/*3 genotypes) status (OR=1.744, 95% CI: 1.360‑2.237, p<0.001) was independently associated with MVCD. The combined impaired CYP2C19 metabolic phenotype (intermediate (*1/*2 and *1/*3 genotypes) plus poor metabolizers) was also independently correlated with MVCD (adjusted OR=1.285, 95% CI: 1.095-1.508, p=0.002). Clinical metabolic comorbidities and the combined impaired CYP2C19 metabolic phenotype are associated with MVCD. These findings may provide valuable reference for risk assessment of severe CAD.

PMID 42763678
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PubMedAsian Pacific journal of allergy and immunology2026-09-20

Type 2-interferon imbalance in allergic barrier disease: An asthma-centered, cross-disease perspective.

Rao Shenghong S, Li Shumei S, Shen Haoyue H, Jin Tengchuan T

Allergic diseases are typically regarded as type 2 inflammatory disorders driven by interleukin-4, interleukin-5, and interleukin-13, which mediate immunoglobulin E class switching, eosinophilic inflammation, mucus hypersecretion, pruritus, tissue remodeling, and epithelial barrier dysfunction. However, type 2 cytokine activity alone does not fully account for variations in exacerbation risk, susceptibility to infections, comorbidities, or responses to biologic therapy. This narrative review proposes an asthma-centered type 2-interferon imbalance framework and discusses its cautious, disease-specific extension to atopic dermatitis, chronic rhinosinusitis with nasal polyps, eosinophilic esophagitis, and food allergy. The model emphasizes that, particularly in asthma, allergic barrier inflammation arises and persists in injured tissues where excessive type 2 inflammation may coexist with impaired interferon-mediated host defense. Evidence is strongest in asthma, where deficiencies in type I and type III interferon responses are linked to rhinovirus susceptibility, delayed viral clearance, and recurrent exacerbations. In other allergic diseases, interferon dysfunction appears more variable, reflecting differences in tissue context, disease stage, and environmental exposure. In asthma, and potentially in selected allergic barrier diseases, persistent inflammation may result from a cycle of epithelial injury, alarmin release, cytokine amplification, impaired antiviral defense, ongoing exposure, and incomplete tissue repair. These mechanisms provide a rationale for tiered intervention, including blockade of upstream epithelial alarmins, inhibition of downstream type 2 effector pathways, and selected investigational approaches aimed at restoring mucosal host defense.

PMID 42763805
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PubMedWellcome open research2026-09-20

The genome sequence of Petasites hybridus (L. G.Gaertn., B.Mey. & Scherb., 1802) (Asterales: Asteraceae).

Ruhsam Markus M, Hollingsworth Peter M PM, Royal Botanic Garden Edinburgh Genome Acquisition Lab, Plant Genome Sizing Collective et al.

We present a genome assembly of Petasites hybridus (Butterbur; Streptophyta; Magnoliopsida; Asterales; Asteraceae). The assembly consists of two haplotypes with total lengths of 2 802.87 megabases and 2 756.82 megabases. Most of haplotype 1 (95.61%) is scaffolded into 30 chromosomal pseudomolecules. Haplotype 2 was assembled to scaffold level. The mitochondrial sequence has a length of 302.34 kilobases and the plastid genome assembly has a length of 150.22 kilobases. Gene annotation of this assembly on Ensembl identified 41 187 protein-coding genes. This assembly was generated as part of the Darwin Tree of Life project, which produces reference genomes for eukaryotic species found in Britain and Ireland.

PMID 42763462
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PubMedBritish journal of cancer2026-09-20

TSPAN32 enhances CAR-T cell potency by assembling IL-2 receptor complex and amplifying its intracellular signal transduction.

Sun Yuanyuan Y, Qiu Qiang Q, Wang Bochuan B, Feng Yunyu Y et al.

Chimeric antigen receptor-engineered T cells (CAR-T) have shown substantial therapeutic potential in hematologic malignancies, but further improvement in T-cell functional capacity is needed to optimize efficacy. We observed reduced TSPAN32 expression in T cells from peripheral blood of patients with B-cell lymphoma. This study aimed to investigate whether TSPAN32 enhances CAR-T cell antitumor activity and to explore the underlying mechanism. TSPAN32 expression was assessed in T cells isolated from patients with B-cell lymphoma. T cells were engineered to co-express TSPAN32 and CD19-CAR, and their antitumor efficacy and cytokine secretion were evaluated in vitro and in subcutaneous tumor models in vivo. Gene expression profiling was performed to identify signaling pathways associated with TSPAN32 overexpression. Mechanistic studies examined the interaction between TSPAN32 and CD25 and its effect on IL-2 signaling. In addition, a transgenic mouse model with endogenous TSPAN32 overexpression and a TSPAN32-specific antibody (FF-37) were used to assess therapeutic potential. TSPAN32 expression was reduced in T cells from B-cell lymphoma patients. Co-expression of TSPAN32 with CD19-CAR significantly enhanced antitumor activity and cytokine production compared with CD19-CAR alone in vitro. In vivo, T cells engineered with both CAR and TSPAN32 showed superior therapeutic efficacy in subcutaneous tumor models. Gene expression profiling indicated increased IL-2 signaling activation in TSPAN32-high CAR-T cells. Mechanistically, TSPAN32 interacted with CD25, promoting its aggregation on the T-cell surface and enhancing IL-2 signal transduction. Endogenous TSPAN32 overexpression in transgenic mice increased resistance to subcutaneous tumor growth. Furthermore, the TSPAN32-specific antibody FF-37 increased TSPAN32 expression and improved CAR-T antitumor efficacy. TSPAN32 enhances CAR-T cell antitumor function by promoting CD25 aggregation and IL-2 signaling activation. Increasing TSPAN32 expression, either through genetic engineering or the TSPAN32-specific antibody FF-37, may represent a promising strategy to improve CAR-T cell therapy.

PMID 42763309
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PubMedCureus2026-09-20

Effectiveness of Structured Education Programmes on Diet and Exercise for Preventing Type 2 Diabetes in Adults With Prediabetes: A Systematic Review.

Muoghalu Chioma G CG, Nwafor Geraldine Ifeoma GI, Onyegbule Chidinma C, Ofoegbu Cosmas C CC et al.

Diet and exercise can prevent or delay progression from prediabetes to type 2 diabetes mellitus, but lifestyle advice in routine care may be brief, inconsistent, or unstructured. This systematic review assessed whether structured education programmes on diet and exercise are more effective than usual care, standard advice or less intensive lifestyle intervention in preventing or delaying type 2 diabetes among adults with prediabetes. The review was conducted in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidance and registered in PROSPERO (CRD42023484038). CINAHL (Cumulative Index to Nursing and Allied Health Literature), Embase, Ovid MEDLINE, Web of Science and Google Scholar were searched for English-language studies from database inception to July 2026. Randomised and cluster-randomised controlled trials involving adults with prediabetes, impaired glucose tolerance, or impaired fasting glucose were included if they compared structured education focused on diet, exercise or both with usual care, standard advice or a less intensive intervention. Data were synthesised narratively. Eighteen randomised or cluster-randomised controlled trials met the inclusion criteria. Most studies reported favourable effects of structured education on diabetes incidence, glycaemic indices and weight-related outcomes compared with usual care or less intensive lifestyle advice, while effects on cardiovascular risk markers were less consistent. Structured education on diet and exercise appears more effective than usual care or less intensive lifestyle advice in preventing or delaying type 2 diabetes among adults with prediabetes.

PMID 42763677
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