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UR

urea (Emolienta / urea, Vinas)

✓ Approved

Vinas · Small Molecule · Small Molecule

What is urea?

urea is a small molecule developed by Vinas. It is approved for therapeutic indications via topical.

Drug Profile

Brand NamesEmolienta, urea, Vinas
CompanyVinas
Drug ClassSmall Molecule
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Vinas

Therapeutic Indications

urea is developed for 4 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersDermatitis allergic✓ Approved
Skin and subcutaneous tissue disordersDermatitis atopic✓ Approved
Skin and subcutaneous tissue disordersDermatitis contact✓ Approved
Skin and subcutaneous tissue disordersPsoriasis✓ Approved

Related Research Articles

PubMedChemSusChem2026-05-24

The Last Frontiers and Challenges in Urea Electrochemical Production Using Carbon Dioxide and Nitrate.

Bani Alessandro A, Muhyuddin Mohsin M, Mustarelli Piercarlo P, Termopoli Veronica V et al.

To reach complete decarbonization by 2050, much effort must be devoted to the electrification of hard-to-abate sectors and the substitution of fossil fuels with renewable sources. Currently, one of the most polluting sectors is the ammonia production through the Haber-Bosch process which is energy-intensive. Moreover, the hydrogen needs to produce ammonia derived from steam reforming of methane gas and the water shift reaction, in turn consuming fossil fuels and emitting more than 2% of the CO2 globally. Ammonia is the building block to produce urea which is the most used nitrogen-containing fertilizer. In the past few years, urea electrosynthesis starting from CO2 and nitrate has captured significantly the interest of the scientific community as it could become the cornerstone to achieve an intense and resilient urea production to reduce emissions and avoid usage of fossil fuels. Here, we discuss the status of the latest achievements in this field, focusing on the reaction mechanisms, different types of electrocatalysts and catalysis pursued, and the detection of urea and their intermediates using a plethora of diverse instruments and methods. This review points out the most critical aspects for research and highlights the potential routes for overcoming the main issues to be solved.

PMID 42177631
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PubMedMetabolomics : Official journal of the Metabolomic Society2026-05-24

Effect of TMEM18 rs7561317 on metabolome in context of obesity.

Farooq Sabiha S, Rana Sobia S, Siddiqui Amna Jabbar AJ, Iqbal Ayesha A et al.

TMEM18 has been indicated by genome-wide association studies as a key gene linked to obesity, yet its exact function and connections with major metabolic networks are unknown. The current study is aimed to determine whether the TMEM18 rs7561317 polymorphism linked with anthropometric indicators of obesity is accompanied with alterations in serum metabolites. This was a case-control study in which a total of 542 participants (Pakistani nationals) were involved including overweight or obese cases and those having normal body mass index (BMI). All participants provided blood samples which were utilized to extract serum and genomic DNA. The genomic DNA of all participants was genotyped for the TMEM18 rs7561317 variant while their serum samples were subjected to untargeted gas chromatography-mass spectrometry based metabolomics. A total of 42 putatively annotated metabolites were selected for further statistical analyses. Analyses revealed that the TMEM18 gene variant (rs7561317) exhibited statistically significant association with five metabolites namely urea, eicosane, geraniol, pentadecanoic acid and porphine as well as with BMI, percent body fat, waist circumference and weight. The G allele of this variant appears to increase the risk of developing overweight or obesity and may be associated with metabolite alterations. The findings highlight the role of metabolite alterations in the manifestation of obese phenotype among individuals carrying the GG genotype of the TMEM18 rs7561317 variant.

PMID 42177698
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PubMedBioorganic chemistry2026-05-24

Chalcogenated phosphine derivatives as urease inhibitors for agricultural: soil application and biophysical studies.

Enes Karine Braga KB, Santos Emeson Farias A EFA, Viana Luciana Pereira Silva LPS, Júnior Marcondes M O MMO et al.

Urease, a metalloenzyme that catalyzes urea hydrolysis, is associated with nitrogen losses in soils. In agricultural settings, although the commercial inhibitor N-(butyl)thiophosphoric triamide (NBPT) is widely used, its low stability under adverse environmental conditions has prompted the search for new, more selective, and stable inhibitors. In this study, triphenylphosphine derivatives functionalized with chalcogens (SF1-SF3) and the corresponding precursor (SF4) were investigated for the ability to transiently inhibit urease catalytic activity. These compounds were tested against urease from Canavalia ensiformis and against soil with varying physicochemical properties. Classic kinetic assays and biophysical studies of urease-ligand interactions were carried out to investigate the mechanisms of urease inhibition. Even in the presence of humic substances, the selenium-containing derivative SF3 was the most effective urease inhibitor among the tested compounds, regardless of soil type. SF3 works as a typical uncompetitive inhibitor, likely by interacting with free cysteine residues located in the flap region near the active site. In situ spectroscopic evidence shows that SF3 may react with cysteine residues to form SF1 and H2Se. Molecular fluorescence approaches demonstrated that SF3 spontaneously interacts with urease and with urease-SF3 via static quenching, driven by electrostatic interactions. These findings highlight SF3 as a promising candidate for application as a urease inhibitor in enhanced-efficiency fertilizers.

PMID 42176360
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-05-24

Short-term actions of arsenic trioxide on metabolic fluxes in the isolated perfused rat liver.

de Queiroz Eskuarek Melo Nairana Mithieli NM, Peralta Rosane Marina RM, Bracht Lívia L, Bracht Adelar A

Arsenic trioxide has recently been approved for the treatment of acute promyelocytic leukemia, but it is also a highly toxic compound. The purpose of the present work was to obtain a general view about the acute effects of arsenic trioxide on liver metabolism using the isolated perfused rat liver, a system that preserves microcirculation and cell polarity. Hepatic lactate and alanine gluconeogenesis were inhibited by arsenic trioxide with IC50 values of 21.7 and 21.4 µM, respectively. Oxygen uptake was inhibited only at concentrations above the IC50 value for gluconeogenesis inhibition. In addition to the carbon fluxes derived from alanine metabolism, arsenic trioxide also inhibited nitrogen detoxification (urea production) with an IC50 of 47.9 µM. Glycolysis from endogenous glycogen was stimulated at concentrations of up to 25 µM. Fructose metabolism was also affected: transformation into glucose was inhibited and fructolysis was stimulated. Glycerol metabolism was not modified. The ATP levels were not significantly diminished, but arsenic trioxide inhibited pyruvate carboxylase and phosphoenolpyruvate carboxykinase, phenomena that seem to be the main cause for gluconeogenesis inhibition. The acute effects of arsenic trioxide described herein are likely to contribute significantly to the general toxicity of the compound especially when combined with the reported long-term induction of exacerbated reactive oxygen species (ROS) production. When using the compound as a therapeutic agent, extreme care must be taken to avoid even mild overdosing as harmful and therapeutic levels for acute promyelocytic leukemia treatment are in fact relatively close to each other.

PMID 42176041
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PubMedThe Journal of nutrition2026-05-24

Dendrobium huoshanense Leaf Flavonoid Extract Ameliorates Hyperuricemia in Mice.

Han Shuo S, Li Chengwang C, Zhang Jie J, Luo Shengyong S et al.

Hyperuricemia is a chronic metabolic disorder posing serious health risks. Dendrobium huoshanense stems are widely used as medicine and functional food ingredients, but the leaves remain underutilized, and their health potential remains unexplored. In this research, the anti-hyperuricemic efficacy and mechanism of Dendrobium huoshanense leaf flavonoid extract (DLFE) are investigated. Hyperuricemia was induced in male Kunming mice (20-25 g, n = 6 per group) by yeast extract. Mice were treated with benzbromarone (BEN, positive control) or DLFE (100 (L), 200 (M), 400 (H) mg/kg/d) for 14 consecutive days. The anti-hyperuricemic effects of DLFE were assessed by measuring serum uric acid (UA), blood urea nitrogen (BUN), serum creatinine (Cr), and hepatic xanthine oxidase (XOD) activity. Renal histology, kidney injury markers (Kim-1, NGAL), inflammatory cytokines (IL-1β, TNF-α), and urate transporters (URAT1, GLUT9, ABCG2) were assessed. Additionally, the underlying mechanisms were elucidated using network pharmacology and subsequently verified in vivo and in vitro. DLFE significantly reduced serum UA (M,136.99 μmol/L and H, 121.99 μmol/L vs HUA, 228.06 μmol/L, p < 0.01), Cr (M, 115.75 μmol/L and H, 99.58 μmol/L vs HUA, 161.90 μmol/L, p < 0.01 and p < 0.001, respectively), BUN (M, 9.82 μmol/L and H, 3.46 μmol/L vs HUA, 13.21 μmol/L, p < 0.01 and p < 0.001), and hepatic XOD activity (M, 25.80 U/L and H, 18.63 U/L vs HUA, 37.59 U/L, p < 0.01 and p < 0.001), mitigated renal injury and decreased Kim-1, NGAL, IL-1β, and TNF-α levels. Moreover, DLFE downregulated URAT1 and GLUT9 expression and upregulated ABCG2 expression. Network pharmacology predicted that DLFE alleviates hyperuricemia primarily by targeting the PI3K/Akt pathway, which was confirmed by reduced PI3K and Akt phosphorylation in mouse renal tissue and HK-2 cells. These findings show that DLFE alleviates hyperuricemia not only by inhibiting hepatic XOD activity to reduce UA production, but, more importantly, by accelerating renal UA excretion via inhibiting the PI3K/Akt pathway to regulate renal UA transporters. Thus, DLFE shows promise as a potential functional food or dietary supplement for hyperuricemia prevention.

PMID 42176988
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PubMedCancer letters2026-05-23

Metabolic Checkpoint CPS1 Sustains TCA Anaplerosis via Urea Cycle in IDH-Mutant Gliomas.

Xu Hao H, Zhang Licheng L, Fu Minjie M, Yang Hui H et al.

Isocitrate dehydrogenase-mutant (IDH-MUT) gliomas exhibit distinct metabolic profile marked by 2-hydroxyglutarate (2-HG) accumulation at the expense of α-ketoglutarate. How these tumors maintain the tricarboxylic acid (TCA) cycle, however, remained unclear. We conducted comprehensive metabolomic profiling using clinical cohorts, cell lines, and patient-derived organoids (PDOs). The metabolic dynamics of TCA and urea cycles were interrogated using stable isotope tracing with 13C-aspartate, U5-13C-15N-aspartate, 15NH4Cl and 15N-glutamate. The functional role of carbamoyl-phosphate synthase 1 (CPS1), the key enzyme of the urea cycle, was validated through inhibition experiments in vitro, in vivo and in PDO model, followed by seahorse respirometry and electron microscopy. Metabolomic profiling of two glioma cohorts consistently showed elevated urea cycle metabolites in IDH-MUT tumors. We identified CPS1 as a metabolic checkpoint sustaining TCA cycle through half urea cycle (from ammonia to arginine). Of note, CPS1 upregulation drove fumarate anaplerosis to sustain TCA flux in IDH-MUT gliomas. Thus, CPS1 inhibition not only reduced fumarate levels but also decreased oncometabolite 2-HG both in vitro and in vivo. Consistently, CPS1 inhibition impaired mitochondrial respiration and suppressed tumor growth in vitro, in vivo and in PDOs. Taken together, metabolic checkpoint CPS1 orchestrates half urea cycle to replenish the TCA cycle in IDH-MUT gliomas. Targeting CPS1 represents a promising metabolic therapeutic target for this glioma subtype.

PMID 42173273
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