UH15-38 TFA
Based on 1 publication(s) in Google Scholar
UH15-38 TFA is a potent RIPK3 inhibitor with an IC50 value of 20 nM. UH15-38 TFA blocks IAV (influenza A virus)-activated necroptosis. UH15-38 TFA dampens IAV-induced lung injury.
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- Pureté : 99.77%
- Formule: C28H28F3N5O4
- Masse moléculaire:555.55
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Stockage:
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
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Chemical Information
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Publications Citing Use of MedChemExpress (MCE) UH15-38 TFA
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Cell Proliferation/Viability Assay
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RT-PCR
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Activité biologique
Description
IC50 & Target
[1]|
RIPK3 20 nM (IC50) |
In Vitro
UH15-38 (0-1000 nM; 12 h) TFA decreases the expression of pMLKL induced by TCZ in a dose-dependent manner[1].
UH15-38 (0-1000 nM) TFA protects type I alveolar epithelial cells from canonical TNF-induced necroptosis and prevents IAV-induced necroptosis[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:Mouse embryonic fibroblasts
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Concentration:0, 25, 50, 100, 250, 500, 750, 1000 nM
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Incubation Time:12 h
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Result:Decreased the expression of pMLKL induced by TCZ (mouse TNF (100 ng/ml), cycloheximide (250 ng/ml) and zVAD (50 μM)) in a time dependent manner.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57Bl/6 mice (lethal dose of PR8 (6,000 × EID50))[1]
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Dosage:30 mg/kg
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Administration:I.p.; once daily for 4 days; starting 24 h after infection
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Result:Markedly reduced numbers of pMLKL+ necroptotic cells, decreased in diffuse alveolar damage and the formation of hyaline membranes, reduced the extent of fibrotic lung damage, displayed significantly lower levels of the pro-fibrotic mediators (IL-1β, IL-6, IL-18, IL-17 and CCL5).
Chemical Information
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Appearance Solid
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Masse moléculaire 555.55
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Formule C28H28F3N5O4
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Color Off-white to light yellow
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SMILES
CN1CCN(CC1)C2=CC(NC3=NC=C4C=C(C(N(C4=C3)C)=O)C5=CC(O)=CC=C5)=CC=C2.O=C(C(F)(F)F)O
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
-20°C, sealed storage, away from moisture and light
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture and light)
Publications (1)
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Journal Impact Factor
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Most Recent
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Transbound Emerg Dis
Activation of ZBP1/RIPK3/MLKL-Dependent Necroptosis by Pseudorabies Virus Restricts Viral Infection in BV2 Microglia Cells. [Abstract]2025 Oct 7:2025:8510846. PMID: 41098523
UH15-38 TFA purchased from MedChemExpress. Usage Cited in: Transbound Emerg Dis. 2025 Oct 7:2025:8510846. [Abstract]
Cell viability of PRV-infected BV2 microglial cells treated with UH15-38 (0.01, 0.1, 1 μM).
UH15-38 TFA purchased from MedChemExpress. Usage Cited in: Transbound Emerg Dis. 2025 Oct 7:2025:8510846. [Abstract]
BV2 microglial cells were pretreated with UH15-38 (0.01, 0.1, 0.5 μM) for 1 h and then infected with PRV for 24 h. The IFN-β, ISG15, and Mx2 mRNA levels were measured by qRT-PCR.
UH15-38 TFA purchased from MedChemExpress. Usage Cited in: Transbound Emerg Dis. 2025 Oct 7:2025:8510846. [Abstract]
BV2 microglial cells were pretreated with UH15-38 (0.01, 0.1, and 0.5 μM) for 1 h, and then PRV JS-2012 was used to infect BV2 microglial cells for 24 h. Then, PRV gE expression levels were analyzed by western blot.
UH15-38 TFA purchased from MedChemExpress. Usage Cited in: Transbound Emerg Dis. 2025 Oct 7:2025:8510846. [Abstract]
BV2 microglial cells were pretreated with UH15-38 (0.01, 0.1, and 0.5 μM) for 1 h, and then PRV JS-2012 was used to infect BV2 microglial cells for 24 h. The expression of PRV gE and p-RIPK3 was visualized by IFA.
Protocole
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Inhalation Toxicity Study
Inhalation toxicity studies expose rodents to a controlled aerosol, vapor, gas, or smoke atmosphere and assess respiratory and systemic toxicity using exposure-atmosphere characterization, clinical observations, body and organ weights, bronchoalveolar lavage fluid, histopathology, blood chemistry, hematology, and, when included, molecular endpoints such as transcriptomics, proteomics, lipidomics, or tissue burden analysis. The primary biological readouts are airway irritation, pulmonary inflammation, cytotoxicity, altered surfactant or lipid homeostasis, impaired particle clearance, and tissue remodeling, reflected by BALF cell differentials, BALF protein, LDH, phosphatase activities, cytokines, lung weight, microscopic respiratory-tract lesions, and retained lung burden.
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
UH15-38 TFA Related Classifications
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