Ask about this productRelated genes to: DHODH Blocking Peptide
- Gene:
- DHODH NIH gene
- Name:
- dihydroorotate dehydrogenase (quinone)
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-29
- Date modifiied:
- 2015-09-11
Related products to: DHODH Blocking Peptide
Related articles to: DHODH Blocking Peptide
- Dihydroorotate dehydrogenase (DHODH), a key enzyme in the de novo pyrimidine biosynthesis pathway of phytopathogenic fungi, has emerged as a promising target for fungicide discovery. In this study, compound VS-24 was identified from a commercial chemical library using molecular docking-based virtual screening and bioactivity assays. Antifungal tests demonstrated that at a concentration of 50 mg/L, VS-24 has broad-spectrum inhibitory effects with inhibition rates of 96.0%, 76.7%, 75.3%, and 76.5% against Valsa mali, Botrytis cinerea, Gaeumannomyces graminis, and Magnaporthe oryzae, respectively. Furthermore, VS-24 provided 45.1% protection against V. mali on apple branches at a concentration of 200 mg/L. Enzyme inhibition assays confirmed its potent inhibitory activity against DHODH. Molecular docking and dynamics simulations further revealed stable binding interactions between VS-24 and DHODH. This study identifies VS-24 as a valuable hit compound, which provides a foundation for developing novel DHODH inhibitors to control plant fungal diseases. - Source: PubMed
Lin Guo-TaiWu Jia-QiZhu Jia-YiYin Ming-HuiLuo LiXu DanLiu XiliXu Gong - Anti-CD20 monoclonal antibodies are highly effective disease-modifying therapies for relapsing multiple sclerosis (RMS), but their comparative efficacy and safety versus teriflunomide, a dihydroorotate dehydrogenase inhibitor, remain clinically important. Teriflunomide is an oral platform treatment with moderate efficacy and a favorable administration profile, making it a relevant comparator for evaluating the benefit-risk profile of anti-CD20 therapies. - Source: PubMed
Publication date: 2026/09/07
Haris Hafiz MuhammadUllah Hafiz AsadGhouri Gul SherHassan AliMaqsood WaleedZaffar ZainabFatima ImanLaiba FnuTariq RishmailWaleed Khan MuhammadQamar SakeenaKhan UroojUmair Sarwar MuhammadIqbal AsmaHussain Bokhari Syed Faqeer - Neurological disorders, including ischaemic and haemorrhagic stroke, traumatic brain injury, and chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, represent a major global health burden. Despite diverse etiologies, these conditions share common pathological mechanisms driven by oxidative stress, neuroinflammation, mitochondrial dysfunction, iron dysregulation, and secondary neuronal injury. The nuclear factor erythroid 2-related factor 2 (Nrf2) signalling cascade and its downstream target heme oxygenase-1 (HO-1) are master regulators of cellular redox homeostasis. HO-1 plays a pivotal yet dichotomous role: its products biliverdin/bilirubin and carbon monoxide exert antioxidant, anti-inflammatory, and anti-apoptotic effects, whereas excessive HO-1 induction can exacerbate iron-mediated oxidative injury and ferroptosis through the release of redox-active ferrous iron. Rather than cataloguing protective studies, this review builds a contextual framework that specifies when HO-1 activation is protective versus detrimental, organised around three converging determinants: cell-type specificity, iron-handling capacity, and disease stage. We extend this framework to the often-overlooked dimensions of sex, age, and model heterogeneity, and use it to interrogate conflicting findings across the literature. We further dissect how Nrf2/HO-1 regulates ferroptosis through the GPX4-ACSL4-SLC7A11 axis, critically appraise the largely unexamined relationship between Nrf2 and the parallel FSP1/CoQ10, GCH1/BH4, and DHODH defence systems, and distil lessons from clinical trials of Nrf2 activators. The goal is an analytical account that identifies where the evidence is robust, where it is contradictory, and where the principal research gaps lie. - Source: PubMed
Publication date: 2026/09/05
Premchandani TanviQutub MohammadThave TejaswiniTaksande JayshreeTatode AmolUmekar Milind - High metabolic heterogeneity and plasticity of triple-negative breast cancer (TNBC) contribute to therapy resistance, necessitating identification of therapeutic vulnerabilities. Here, we identify non-canonical functions of the extracellular matrix (ECM) remodeler, lysyl oxidase (LOX), in regulating glucose metabolism and mitochondrial homeostasis and show that inhibiting LOX generates targetable vulnerability to ferroptosis. Mechanistically, LOX interacts with PARKIN and its upstream kinase PINK1, which we identified as a substrate of LOX. LOX-mediated PINK1 oxidation suppresses PARKIN phosphorylation, stabilizing hypoxia-inducible factor 1-alpha (HIF-1α) and increasing glycolysis. Concomitantly, LOX inhibits PARKIN-mediated mitophagy and maintains mitochondria-ER contacts through VDAC1 stabilization, while the LOX-HSP90 complex promotes mitochondrial Ca transport and ATP production. Inhibiting LOX suppresses glycolysis, disrupts mitochondrial dynamics, reduces OXPHOS and GPX4/FSP1, and induces compensatory DHODH activity. Our "one-two punch" approach combining LOX inhibition with clinical DHODH inhibitor suppresses tumor growth in vivo in chemo-free setting. Notably, LOX protein correlates with HIF-1α/GLUT1/GPX4 in TNBC patient tumors, supporting its clinical relevance. - Source: PubMed
Publication date: 2026/08/31
Saatci OzgeUlukan BurgeCetin MetinKuasne HellenMartinez ConstanzaPercin ElifOleinik NataliaSavoca Matthew TNehme AliHernández-Corchado AldoZavacky EvelynSreenivas KukkamudiRezaeian Abdol HBethard Jennifer RAnoma Jean-SebastienSahin Ozlem SenerAguilar-Mahecha AdrianaBuchanan MargueriteAras MertkayaDeBlois GenevieveBasik MarkHill Elizabeth GBall Lauren ERao Chintada NageswaraMcInnes CampbellRiazalhosseini YasserNajafabadi Hamed SLemasters John JOgretmen BesimPark MoragSahin Ozgur - Leishmaniasis is one of the most prominent worldwide flagellated protozoan parasite diseases. Natural products have gained attention as potential anti-leishmanial agents due to their fewer side effects, low toxicity, and cost effectiveness compared to conventional chemotherapy drugs. In the current study, the network pharmacology approach was used to evaluate the therapeutic potential of derived phytochemicals against Leishmaniasis and toidentify potential anti-leishmanial agents targeting key proteins implicated in leishmaniasis progression.To carry out this study, several databases including Cytoscape, IMPPAT, Dr. Duke's, Kyoto Encyclopaedia of Genes and Genomes (KEGG), and STRING database, were used to conduct network pharmacology to examine the biomolecular approach of metabolites of the plant in leishmaniasis disease. A total of 33 phytochemical components from were analyzed, resulting in the identification of five major bioactive molecules: betulinic acid, betulin, lupeol, oleanolic acid, and karachic acid. These compounds had high affinity for a variety of leishmaniasis-related molecular targets, including MAPK1, NFKB1, TLR4, HSD17B10, and DHODH, among others. A protein-protein interaction (PPI) network was created to identify essential connections, and Gene Ontology (GO) and KEGG pathway enrichment studies revealed their involvement in inflammation, immunological regulation, and apoptotic pathways. Among these metabolites, betulin and betulinic acid were found to be the most active metabolites with the most prominent interaction with the genes that play an active role in the pathophysiology of leishmaniasis. may be identified potential source of anti-leishmanial drug candidates. - Source: PubMed
Publication date: 2026/01/06
Loshali AanchalSaifi SumailaJoshi Bhuwan ChandraBawa SandhyaAeri Vidhu