TPT-260
Based on 2 publication(s) in Google Scholar
TPT-260 (TPU260), a thiophene thiourea derivative, is a retromer complex stabilizer against thermal denaturation (Kd = ~5 µM). TPT-260 increases the levels of retromer proteins, shifts amyloid-precursor protein (APP) away from the endosome, and decreases the pathogenic processing of APP. TPT-260 inhibits TLR4 upregulation, IKKβ phosphorylation, NF-κB p65 nuclear translocation, and NLRP3 inflammasome formation. TPT-260 improves retromer-mediated cargo trafficking, reduces brain infarct area, and decreases amyloid plaque deposition. TPT-260 exhibits minimal cytotoxicity to primary microglia at tested concentrations. TPT-260 can be used for the research of inflammatory bowel disease, ischemic stroke and Alzheimer's disease.
For research use only. We do not sell to patients.
- CAS No.: 769856-81-7
- Formula: C8H12N4S3
- Molecular Weight:260.40
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) TPT-260
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Biological Activity
TPT-260 (10 μM) improves Occludin recycling and epithelial barrier function in Caco-2 cells but has no effect on VMP1-knockdown Caco-2 cells, indicating VMP1 is required for the Target Reagent's activity[1].
TPT-260 (5-20 μM) has no cytotoxic effect on primary mouse microglia, as measured by cell viability and LDH release assays[2].
TPT-260 (5-20 μM) protects primary mouse microglia from LPS (HY-D1056)/Nigericin (HY-127019)-induced cytotoxicity, as shown by restored cell viability and reduced LDH release[2].
TPT-260 (5-20 μM) inhibits LPS/Nigericin-induced inflammasome formation in primary mouse microglia, as measured by reduced ASC speck formation[2].
TPT-260 (5-20 μM) inhibits LPS/Nigericin-induced nuclear translocation of NF-κB p65 in primary mouse microglia, as measured by reduced nuclear p65 fluorescence intensity[2].
TPT-260 (5-20 μM) inhibits LPS (HY-D1056)/Nigericin (HY-127019)-induced upregulation of pro-inflammatory gene expression (Nlrp3, Tnfa, Il1b) in primary mouse microglia[2].
TPT-260 (5-20 μM) attenuates LPS/Nigericin-induced activation of the TLR4-IKKβ-NF-κB pathway in primary mouse microglia, as shown by reduced levels of pathway-related proteins and pro-inflammatory IL-1β[2].
TPT-260 (5 μM; 48 h) increases plasma membrane expression of NHE3 in Caco-2/bbe cells, raising surface NHE3 to 142.4% of control[3].
TPT-260 (5 μM; 48 h) increases levels of core retromer proteins VPS35 and VPS26 in Caco-2/bbe cells, and prevents the Cholera toxin (CT)-induced reduction in these retromer proteins when given either concurrently with CT or prior to CT exposure[3].
TPT-260 (5 μM; 48 h) increases plasma membrane expression of NHE3 in polarized Caco-2/bbe-HA-NHE3 cells, and reverses the CT-induced reduction in NHE3 surface expression when given either concurrently with CT or prior to CT exposure[3].
TPT-260 (5 μM; 48 h) partially reduces forskolin-induced fluid secretion in 3D human duodenal enteroids by stimulating NHE3-mediated fluid absorption[3].
TPT-260 (R55) binds to retromer complex with a Kd of ~5 μM[4].
TPT-260 (48 h) increases Vps35 levels with an EC50 of ~3.3 μM in primary hippocampal neurons[4].
TPT-260 (48 h) significantly reduces the levels of both endogenous Aβ40 and Aβ42 in hippocampal neurons[4].
TPT-260 inhibits Aβ levels with an IC50 of ~12 μM in hippocampal neurons[4].
TPT-260 significantly reduces the levels of both endogenous β-CTF and sAPPβ, and increases sAPPα levels in hippocampal neurons[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:Caco-2/bbe cells
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Concentration:5 μM
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Incubation Time:48 h
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Result:Increased amounts of VPS35 to 125% of control and VPS26 to 129% of control when used alone.
Prevented the CT-induced reduction in VPS35 and VPS26 levels, maintaining them at levels similar to untreated controls when given concurrently with CT or before CT.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 (2-month-old) bearing middle cerebral artery occlusion (MCAO) surgery[2]
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Dosage:5 mg/kg
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Administration:i.p.; single dose (24 hours prior to MCAO surgery)
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Result:Significantly improved Bederson score (neurological function) in MCAO mice.
Significantly reduced brain infarct volume on the affected side.
Significantly suppressed brain tissue levels of pro-inflammatory factors IL-1β and TNF-α compared to untreated MCAO mice.
Chemical Information
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CAS No. 769856-81-7
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Molecular Weight 260.40
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Formula C8H12N4S3
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SMILES
NC(SCC1=CC=C(CSC(N)=N)S1)=N
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Synonyms
TPU260
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications (2)
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Journal Impact Factor
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Most Recent
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J Inflamm Res
Therapeutic Potential of TPT-260 in Ischemic Stroke: An Investigation Into Its Anti-Inflammatory Effects and Impact on Microglial Activation. [Abstract]2025 Mar 1:18:3055-3066. PMID: 40046681
Purity & Documentation
References
[1]. Zhao J, et al. Loss of VMP1 Impairs Tight Junction Recycling and Aggravates Intestinal Barrier Dysfunction in Inflammatory Bowel Disease. Adv Sci (Weinh). Published online February 27, 2026. [Content Brief]
[2]. Qian J, et al. Therapeutic Potential of TPT-260 in Ischemic Stroke: An Investigation Into Its Anti-Inflammatory Effects and Impact on Microglial Activation. J Inflamm Res. 2025 Mar 1;18:3055-3066. [Content Brief]
[3]. Singh V, et al. Cholera toxin inhibits SNX27-retromer-mediated delivery of cargo proteins to the plasma membrane. J Cell Sci. 2018;131(16):jcs218610. Published 2018 Aug 17. [Content Brief]
[4]. Mecozzi VJ, et al. Pharmacological chaperones stabilize retromer to limit APP processing. Nat Chem Biol. 2014 Jun;10(6):443-9. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)