Drug Database
TR

travoprost (Travatan Z / Travantan Z / Travatanz)

✓ Approved

Novartis AG · PTGFR · Small Molecule

What is travoprost?

travoprost is a small molecule developed by Novartis AG. It is approved for therapeutic indications via others.

Drug Profile

Brand NamesTravatan Z, Travantan Z, Travatanz
CompanyNovartis AG
Drug ClassSmall Molecule
Molecular TargetPTGFR
RouteOthers
StatusApproved
Sources: ClinicalTrials.gov, Novartis AG

Mechanism of Action

Molecular Targets

travoprost acts on 1 molecular target:

PTGFRprostaglandin F receptor (FP)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Eye disordersGlaucoma✓ Approved

Related Research Articles

PubMedFrontiers in public health2026-09-04

Association between early menopause and adverse cardiovascular events in postmenopausal women: a systematic review and meta-analysis stratified by smoking status and type 2 diabetes mellitus.

Chen Zhongfang Z, Zhang Xinyan X, Chen Yu Y, Shi Wen W et al.

The impact of early menopause on adverse cardiovascular events may be modified by smoking and type 2 diabetes mellitus (T2DM). This study aims to investigate the effect of early menopause on adverse cardiovascular events in women, with stratification by smoking status and T2DM status. Studies were retrieved from four databases (Embase, Web of Science, PubMed, and Cochrane Library) from their inception to January 2026. In this study, early menopause was defined as natural menopause occurring before age 45 years, encompassing both premature menopause (<40 years) and early menopause (40-45 years). This systematic review was registered with PROSPERO (Registration No.: CRD420251238709). Results were presented as hazard ratios (HR) or relative risks (RR) with corresponding 95% confidence intervals (95% CI). In this study, a total of seven cohort studies involving over 1.77 million postmenopausal women were included. Among non-smoking women, early menopause was associated with a higher risk of heart failure (HF: HR = 1.23, 95% CI = 1.02-1.49, p = 0.031, I 2 = 87.9%, n = 2) and coronary heart disease (CHD: RR = 1.26, 95% CI = 1.18-1.35, p < 0.001, I 2 = 0.0%, n = 2). In contrast, among smoking women, we did not find statistically significant evidence of an association between early menopause and either HF (HR = 1.15, 95% CI = 0.88-1.52, p = 0.311, I 2 = 73.7%, n = 2) or CHD (RR = 1.63, 95% CI = 0.90-2.96, p = 0.105, I 2 = 97.2%, n = 2). For women without T2DM, early menopause was associated with a higher risk of both HF (HR = 1.19, 95% CI = 1.00-1.43, p = 0.050, I 2 = 94.1%, n = 2), a borderline finding that should be interpreted with caution, and significantly associated with stroke (HR = 1.11, 95% CI = 1.09-1.13, p < 0.001, I 2 = 0.0%, n = 2). For women with T2DM, early menopause was associated with a higher risk of HF (HR = 1.29, 95% CI = 1.11-1.50, p = 0.001, I 2 = 54.3%, n = 2), but not find with stroke risk (HR = 1.11, 95% CI = 0.99-1.25, p = 0.062, I 2 = 59.6%, n = 2). In both the T2DM and non-T2DM groups, no statistically significant evidence of an association between early menopause and with all-cause mortality was found (T2DM: HR = 1.20, 95% CI = 0.83-1.74, p = 0.333, I 2 = 54.3%, n = 2; without T2DM: HR = 1.18, 95% CI = 0.94-1.47, p = 0.148, I 2 = 53.3%, n = 2, respectively). Early menopause is associated with the risk of adverse cardiovascular events in women, with divergent results by smoking status and T2DM. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251238709; identifier: CRD420251238709.

PMID 42694168
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PubMedIranian biomedical journal2026-09-04

Tropolone Derivative JO-122(2) Enhances Temozolomide Efficacy and p53-Mediated Apoptosis in Glioblastoma Xenografts.

Kit Oleg I OI, Maksimov Aleksey Yu AY, Golovinov Igor V IV, Kuznetsova Natalia S NS et al.

Glioblastoma (GBM) is the most aggressive primary brain tumor in adults, with limited therapeutic options and poor survival. Resistance to standard temozolomide (TMZ) therapy remains a major challenge, necessitating novel agents. Tropolone derivatives, particularly the synthetic trichlorotropolone JO-122(2), have shown broad preclinical antitumor activity. This study aimed to determine whether JO-122(2), alone or combined with TMZ, can suppress GBM growth in vivo and to define the accompanying changes in the p53/MDM2/Bcl-2 apoptotic axis. JO-122(2), as monotherapy or combined with TMZ, was evaluated in a U87 MG GBM xenograft model in BALB/c nude mice (n = 8 per group). Tumor volumes were monitored over 25 days, and tumor growth inhibition (TGI) was calculated. Molecular mechanisms were investigated by RT-qPCR and ELISA, assessing gene expression and protein levels of the apoptotic regulators TP53, MDM2, BAX, BCL2, and CASP9. JO-122(2) and TMZ monotherapy inhibited tumor growth (TGI = 42.08% and 61.44%, respectively). The combination therapy reduced tumor volume 4.9-fold compared to the vehicle control and achieved a TGI of 79.88% (p = 4.20 × 10⁻⁸ vs. control; p = 1.66 × 10⁻³ vs. TMZ; p = 5.97 × 10⁻⁵ vs. JO-122(2)). It also increased p53, Bax, and caspase-9 protein levels and decreased MDM2 and Bcl-2, with concordant upregulation of TP53 and BAX and downregulation of MDM2 and BCL2 mRNA, indicating modulation of the p53/MDM2/Bcl-2 axis. JO-122(2) exerts potent antitumor effects in GBM, particularly when combined with TMZ, by promoting mitochondrial apoptosis through the coordinated regulation of p53 and its downstream effectors.

PMID 42694763
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PubMedAngewandte Chemie (International ed. in English)2026-09-04

Machine Learning-Driven Alloy Anode Accompanied by Interfacial Kinetic Compensation Design Toward High-Rate Zinc Pouch Cells.

Li Mingzhu M, Du Shengwei S, Liang Shuquan S, Wang Xin X et al.

Developing practical aqueous zinc metal batteries is crucial for safe grid energy storage. However, zinc anode imposes severe interfacial mass transfer and kinetic bottlenecks at high rates and high capacities, driven by thermodynamically competitive hydrogen evolution reaction and significant polarization. In this work, we establish a predictive design paradigm that resolves this dilemma by integrating active‑learning materials screening and a composition‑gradient alloy (GL) anode with an interfacial kinetic compensation. Moreover, the gradient grain boundaries preclude structural failure under high capacities arising from stress concentration at high rates. Consequently, GL anode achieves 20,000 cycles at 40 mA cm-2 and the cumulative capacity of 81.36 Ah at 80 mA cm-2. The symmetric cell endures more than 400 h at 80% depth of discharge and 20 mA cm-2, while pouch cells exceed 1000 h at 5 mAh cm-2. Coupled with high-loading vanadium-based cathode (30 mg cm-2, 4.5 mAh cm-2), the full cell retains 91% capacity after 1500 cycles. Notably, a 560 mAh pouch cell stable for 350 cycles over 90% capacity retention at a high rate of 20 mA cm-2. This work offers a design concept of practical zinc anode with high-rate stability for zinc pouch cells.

PMID 42694010
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PubMedNature microbiology2026-09-04

BCL-2 inhibition at antiretroviral therapy initiation reduces the intact SIV reservoir in macaques.

Wiche Salinas Tomas Raul TR, Harper Justin J, Deleage Claire C, Nguyen Kevin K et al.

The anti-apoptotic molecule BCL-2 favours the maintenance of the CD4+ T-cell reservoir during HIV infection. Whether inhibition of BCL-2 can lead to long-term reduction of the HIV reservoir is unclear. Here we initiated antiretroviral therapy (ART) in 24 simian immunodeficiency virus (SIV)-infected rhesus macaques at 14 days post infection (p.i.), alone or combined with a 10-day treatment of venetoclax or venetoclax and CD8α depletion, with a follow-up to day 294 p.i. We report a rapid and sustained reduction of the intact SIV reservoir in venetoclax-treated rhesus macaques in blood and lymph nodes. CD4+ T cells that persisted after venetoclax treatment showed partial reduction in apoptotic sensitivity in ex vivo assays. These exhibited elevated expression of anti-apoptotic BCL-2 and BCL-xL, and showed reduced expression of pro-apoptotic molecules such as PUMA. These findings support the rationale for extended venetoclax dosing and suggest that combining BCL-2 inhibition with agents targeting additional anti-apoptotic molecules could enhance clearance of the viral reservoir in HIV cure strategies.

PMID 42693271
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PubMedEcology and evolution2026-09-04

Estimating Area of Occupancy From Incomplete Occurrence Records: Reproducible Workflow Illustrated on a Comprehensive Dataset of Georgian Snakes.

Iankoshvili Giorgi G, Tarkhnishvili David D

Area of occupancy (AOO) is a widely used metric for assessing species' vulnerability. To standardize AOO estimation, the IUCN recommends using a fixed 2 × 2 km grid. However, for species represented by sparse and irregular records, this resolution can substantially underestimate AOO. Although spatial modeling offers a potential solution, model-based estimates may differ among taxa and studies depending on data structure, predictor choice, and modeling strategy. In this paper, we present a reproducible workflow that uses breakpoint analysis of record-accumulation curves to identify informative species-specific grid sizes and to estimate AOO from incomplete occurrence records. We applied this framework to 13 snake species found in Georgia, with diverse ecological characteristics within a topographically complex, irregularly sampled region. Repeated subsampling of the six best-represented species showed that accumulation-curve predictions were more accurate than raw occupied-cell counts in 96%-98% of comparisons. Nine of the 13 species showed significant breakpoint-derived scales between approximately 4 and 13 km rather than at the standard 2 km resolution. This workflow offers a practical way to explore scale dependence, sampling incompleteness, and sensitivity of AOO estimates derived from historical and citizen-science occurrence datasets. The workflow complements the standardized 2 × 2 km AOO used in formal IUCN Red List assessments.

PMID 42694863
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PubMedFrontiers in endocrinology2026-09-04

Disproportionate reporting of euglycaemic and diabetic ketoacidosis with SGLT-2 inhibitors across expanding cardiorenal indications: a cross-database study of FAERS and JADER.

Chen Jinqian J, Wang Deyin D, Duan Xiaochuan X, Wang Jianbo J et al.

SGLT-2 inhibitors are now used beyond type 2 diabetes (T2DM) in heart failure (HF) and chronic kidney disease (CKD), where glucose is monitored less routinely. Whether their established ketoacidosis signal-particularly euglycaemic diabetic ketoacidosis (euDKA)-is maintained as the indications expand, and whether it reproduces across independent reporting systems, is untested. We analysed the US FAERS (2020Q1-2026Q1) and Japanese JADER using one pipeline. Signals required consensus across four methods (ROR, PRR, IC, EBGM/EB05). Analyses were run overall, within report-level indication strata [T2DM, HF, CKD, off-label type 1 diabetes (T1DM)] and against an active comparator (DPP-4 inhibitors), with two pre-specified negative controls, time-to-onset modelling and sensitivity analyses. The DKA signal met four-method consensus within every indication stratum, including HF and CKD, and was highest in off-label T1DM; it was therefore maintained, not diluted, as indications expanded. Overall RORs were 67.4 (95% CI 65.7-69.2) in FAERS and 112.3 (104.8-120.3) in JADER. SGLT-2 inhibitors accounted for 85.8% (FAERS) and 91.7% (JADER) of all euDKA reports, though euDKA was only 4.1% and 7.8% of SGLT-2 inhibitor reports. Both negative controls were null in both databases. Median time-to-onset was 60 days (Weibull β=0.48, 95% CI 0.46-0.50). Across two independent reporting systems, the SGLT-2 inhibitor ketoacidosis signal was maintained across the expanding cardiorenal indications, with euDKA concentrated within this class and early onset. Ketone-based assessment is warranted when ketoacidosis is suspected, particularly soon after initiation. As a disproportionality analysis, these are hypothesis-generating signals that cannot establish incidence, relative risk, or causality.

PMID 42694226
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