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

PubMedOrganic letters2026-11-13

Pinacolborane-Enabled Low-Valent Cobalt Catalysis for Enantioselective [2 + 2 + 2] Cycloaddition of Enediynes.

You Yang'en Y, Ge Shaozhong S

An enantioselective cobalt-catalyzed [2 + 2 + 2] cycloaddition of enediynes has been developed employing Co(acac)2 and (R)-binap activated by pinacolborane (HBpin). This reaction converts a wide range of enediynes into chiral tricyclic cyclohexadienes in high yields with excellent enantioselectivities (up to 99% ee). The cyclohexadiene products can undergo stereospecific Pd-catalyzed hydrogenation to afford chiral cyclohexanes bearing five continuous stereogenic carbon centers with high diastereoselectivity (dr >19:1). Mechanistic studies support a diyne-initiated cobalt(I)-mediated cycloaddition pathway.

PMID 43023901
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PubMedOrganic letters2026-11-13

Palladium-Catalyzed Domino [3 + 2] Cyclization and C-P/C-B Bond Construction Employing (2-Bromoaryl)boronates as C2 Synthons.

Zheng Yiyi Y, Meng Yu Y, Chen Tao T, Cheng Haoyu H et al.

A palladium-catalyzed multicomponent cascade reaction involving o-iodostyrenes, (2-bromoaryl)boronates, and H-phosphonates or bis(pinacolato)diboron has been developed. The reaction features sequential Suzuki-Miyaura coupling, Heck cyclization, and C-P/C-B bond construction, wherein (2-bromoaryl)boronate acts as a dual coupling partner to overcome the inherent regioselectivity limitations of its aryne precursor pathway.

PMID 43023913
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PubMedJournal of virology2026-11-13

Neuropsychiatric long COVID is associated with altered SARS-CoV-2-specific cellular-humoral coordination and diminished EBV-specific humoral immunity up to 12 months post-COVID-19 symptom onset.

Samaan Philip P, Budylowski Patrick P, Matveev Vitaliy V, Russell Victoria V et al.

Long COVID is a chronic multisystemic condition estimated to affect approximately 400 million people worldwide. Although underlying mechanisms remain elusive, persistent SARS-CoV-2 reservoirs and Epstein-Barr virus (EBV) reactivation have been implicated. We compared SARS-CoV-2- and EBV-specific cellular and humoral immunity between 27 long COVID individuals with ≥2 neuropsychiatric symptoms and 27 matched recovered participants at 3-6 months post-COVID-19 symptom onset (PSO). Peripheral blood mononuclear cells were assessed for IFN-γ, IL-2, TNF, and granzyme B T-cell responses against SARS-CoV-2, EBV, and HCMV. Sera were evaluated for neutralizing activity against live ancestral SARS-CoV-2 and EBV, while EBV reactivation was assessed by anti-early antigen-diffuse IgG and anti-viral capsid antigen (VCA) IgM. We observed no significant differences in SARS-CoV-2-, EBV-, or HCMV-specific Th1-type/cytotoxic T-cell responses or live virus neutralization between long COVID and recovered groups at 3-6 months PSO. Although SARS-CoV-2-specific IFN-γ and IL-2 T-cell responses correlated with serological neutralizing capacity in recovered participants, no such associations were observed in the long COVID group, suggesting altered coordination between cellular and humoral immunity. EBV reactivation was only detected in one neuropsychiatric long COVID participant. However, EBV anti-VCA IgG antibody levels were significantly diminished in long COVID participants at 3-6 months PSO. Reports of fatigue at 12 months PSO were also associated with reduced EBV neutralizing capacity at 3-6 months PSO. Diminished EBV-specific humoral immunity and dysregulated coordination between SARS-CoV-2-specific cellular and humoral immunity may thus represent potential prognostic markers for neuropsychiatric long COVID development and fatigue up to 12 months PSO.IMPORTANCEWe performed a comprehensive analysis of cellular and humoral immune responses to SARS-CoV-2, Epstein-Barr virus (EBV), and human cytomegalovirus in individuals with neuropsychiatric long COVID, a subgroup that remains poorly characterized. Although no differences in virus-specific Th1-type or cytotoxic T-cell immunity were observed between individuals with long COVID and recovered individuals, altered coordination between SARS-CoV-2-specific T-cell and neutralizing humoral immunity was observed in the long COVID group at 3-6 months post-COVID-19 symptom onset (PSO). Diminished EBV-specific humoral immunity was also associated with neuropsychiatric long COVID and fatigue up to 12 months PSO. Together, these findings suggest that altered SARS-CoV-2-specific cellular-humoral immune coordination and diminished EBV-specific humoral immunity may contribute to the development or persistence of neuropsychiatric long COVID and highlight a promising future direction for mechanistic studies.CLINICAL TRIALSThis study is registered with ClinicalTrials.gov as NCT05125510.

PMID 43023729
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PubMedNeuro-oncology2026-11-13

Vorasidenib in IDH1/2-mutant low-grade gliomas: a prospective study on volumetric MRI and seizure outcome.

Rudà Roberta R, Bruno Francesco F, Pronello Edoardo E, Pellerino Alessia A et al.

The IDH1/2 inhibitor vorasidenib demonstrated efficacy in residual or recurrent grade 2 IDH1/2-mutant gliomas after surgery. However, there is lack of knowledge regarding factors predicting the probability of response. We conducted a prospective single-centre study on 54 grade 2 IDH1/2-mutant astrocytomas and IDH1/2-mutant 1p/19q-codeleted oligodendrogliomas treated with vorasidenib. MRI response (2D and 3D) and seizure outcome were longitudinally assessed. Factors associated with response were explored using regression models. With a median follow-up of 17.5 months, vorasidenib induced progressive tumour shrinkage on MRI, with median volume reductions of - 12.2% at cycle 6, -27.8% at cycle 12, and -55.5% at cycle 18. Best volumetric response was CR in 1 patient, PR in 5, MR in 9, SD in 31 and PD in 7. The ORR (CR + PR + MR) was 28%. Eighteen patients who had focal grade 3 areas showed similar volumetric response and ORR. 9/12 (75%) patients with baseline seizures achieved ≥50% reduction or seizure freedom. MRI response correlated with early treatment initiation and early seizure reduction. Vorasidenib was generally well tolerated, with liver enzyme elevation being the main adverse event. Vorasidenib induced sustained tumour shrinkage and seizure control. Early treatment initiation and early seizure reduction were associated with MRI response.

PMID 43023458
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PubMedFrontiers in pharmacology2026-11-13

Integrated chemical profiling and lipidomics reveal that Mailuoning oral liquid alleviates diet-induced MASLD via PPARα-mediated lipid homeostasis and COX-2 inhibition, with identification of potential active constituents.

Wu Sijia S, Jia Wangya W, Zhou Xun X, Zhu Linyan L et al.

Mailuoning oral liquid (MLN), a standardized five-herb formula, is used for ischemic vascular diseases and shows potential in ameliorating dyslipidemia. Our previous study showed MLN alleviates metabolic dysfunction-associated steatotic liver disease (MASLD) via peroxisome proliferator-activated receptor α (PPARα) activation, but its comprehensive chemical profile, systemic exposure, and bioactive constituents mediating both PPARα activation and cyclooxygenase-2 (COX-2) inhibition remain unclear. High-fat, high-fructose diet-fed rats received MLN (5.4 or 10.8 mL/kg/day) for 8 weeks. Ultra-high-performance liquid chromatography coupled with Q-Exactive Orbitrap high-resolution mass spectrometry (UHPLC-Q-Exactive Orbitrap HRMS) profiled MLN chemicals and identified serum/liver prototypes. Biochemical profiles, glucose tolerance, histopathology, untargeted lipidomics, and targeted polyunsaturated fatty acid (PUFA) analysis were performed. PPARα and COX-2 signaling were examined by quantitative real-time polymerase chain reaction (qPCR), western blotting, and immunohistochemistry. Key constituents were screened for PPARα activation via dual luciferase reporter assay and molecular docking; COX-2 inhibition was validated by enzyme assays and molecular dynamics. A total of 143 compounds were characterized; 48 and 92 prototypes were enriched in serum and liver, respectively. MLN ameliorated dyslipidemia, glucose intolerance, steatosis, and inflammation. Lipidomics revealed bidirectional modulation of hepatic lipids, reversing triglyceride (TAG) accumulation and restoring phosphatidylcholine (PC) and lysophosphatidylcholine (LPC) levels. Targeted analysis showed increased eicosapentaenoic acid (EPA) and normalized COX-2-derived prostaglandins (PGD2, PGE2). MLN activated hepatic PPARα and downregulated COX-2. Seven serum-enriched compounds (chlorogenic acid, macranthoidin B, luteoloside, harpagide, angoroside C, oleanolic acid, betaine) were validated as direct PPARα agonists. Secologanoside and chikusetsusaponin IVa were identified as novel COX-2 inhibitors (half-maximal inhibitory concentration (IC50) = 14.61 and 120.9 nM). MLN alleviates MASLD via dual PPARα activation and COX-2 inhibition, providing a mechanistic foundation for repurposing this herbal formula in early-stage MASLD.

PMID 43022466
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PubMedFood science and biotechnology2026-11-13

Inhibitory effects of phenylpropionamides from the hemp seed cake on protein tyrosine phosphatase 1B: in vitro, molecular docking, and network pharmacology approach.

Cao Thao Quyen TQ, Yeo Chae Eun CE, Yu Seunguk S, Chi Hae Na HN et al.

Herein, two phenylpropionamides, N-trans-caffeoyltyramine (1) and N-trans-feruloyltyramine (2), were isolated from the hemp seed cake. Their structures were elucidated using spectroscopic analysis and comparison with literature data. Compounds 1 and 2 exhibited the potential inhibitory activity against protein tyrosine phosphatase 1B, with IC50 values of 62.0 and 14.0 μM, respectively. Kinetic analysis showed compound 2 as a mixed inhibitor with a K i of 30.9 μM. Molecular docking analysis demonstrated the potential of 2 to inhibit the PTP1B enzyme, revealing specific interactions between it and target proteins. Additionally, a network pharmacology approach was used to explore the potential molecular mechanisms of 2 for the treatment of type 2 diabetes mellitus. Overall, the findings provide the first evidence of PTP1B inhibitory activity and new insights into the mechanisms of action of phenylpropionamides, suggesting that hemp seed cake is a source of PTP1B inhibitors for further investigation in the context of diabetes research. The online version contains supplementary material available at https://doi.org/10.1007/s10068-026-02293-8.

PMID 43022098
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