TR-100
Based on 1 Customer Validation
TR-100 is a Tpm3.1 inhibitor that binds to and disrupts Tpm3.1-containing Actin filaments, enhancing the depolymerizing effect of Tpm3.1 on actin without altering actin-tropomyosin binding. TR-100 induces actin cytoskeleton rearrangement. TR-100 shortens membrane nanotubes and alters tube thickness in a concentration-dependent manner. TR-100 increases basal insulin secretion and inhibits glucose-stimulated insulin secretion. TR-100 inhibits insulin-stimulated glucose uptake. TR-100 can be used for research on B lymphoma.
For research use only. We do not sell to patients.
- Purity : 99.0%
- CAS No.: 1128165-86-5
- Formula: C26H38N4O
- Molecular Weight:422.61
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| U2OS | IC50 |
10.8 μM
Compound: 12420
|
Inhibition of dynamin 1-mediated endocytosis internalization of Tf-A594 in human U2OS cells pretreated for 30 mins
Inhibition of dynamin 1-mediated endocytosis internalization of Tf-A594 in human U2OS cells pretreated for 30 mins
|
[PMID: 19459681] |
In Vitro
TR100 (25 µM; 1 h) disrupts cortical F-actin in MIN6 β-cells under basal and high glucose conditions[2].
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:MIN6 β-cells
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Concentration:25 µM (TR100); 2.8 mM or 25 mM (glucose)
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Incubation Time:1 h (TR100); 10-30 min after glucose stimulation (fixation)
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Result:Led to significant loss of F-actin at the cell cortex in both basal and glucose-stimulated states.
In Vivo
In Tpm3.1 knockout mice, TR-100 (40 mg/kg BW; i.p.; single injection; 1 h before GTT/ITT) has reduced impact on glucose clearance and does not suppress glucose-stimulated insulin secretion, consistent with on-target Tpm3.1 action[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:wild-type (10-12-week-old male)[2]
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Dosage:40 mg/kg BW
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Administration:i.p.; single injection; 1 h before GTT/ITT
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Result:Had blood glucose similar to vehicle-injected controls one hour after injection.
Decreased glucose clearance.
Suppressed glucose-stimulated insulin secretion completely; insulin levels were not different from baseline at all time points after glucose injection.
Had no impact on insulin-stimulated glucose clearance in the ITT.
Had little effect on glucose clearance at 8 h after administration.
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Animal Model:B6-Tpm3tm2(∆9d)Pgun (10-12-week-old male)[2]
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Dosage:40 mg/kg BW
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Administration:i.p.; single injection; 1 h before GTT/ITT
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Result:Decreased glucose clearance, but the impact was less than in wild-type mice.
Showed glucose-stimulated insulin secretion equivalent to vehicle controls.
Had no impact on insulin-stimulated glucose clearance in the ITT.
Chemical Information
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CAS No. 1128165-86-5
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Appearance Solid
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Molecular Weight 422.61
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Formula C26H38N4O
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Color White to light yellow
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SMILES
O=C(NCCCCCCCC)/C(C#N)=C/C1=C(C)N(CCCN(C)C)C2=C1C=CC=C2
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Protocols
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Research Protocol for Endocrine Diseases
Endocrine diseases often arise from disrupted hormone production, hormone signaling, or target-tissue responsiveness; for diabetes-focused endocrine disease models, insulin signaling regulates glucose uptake, hepatic glucose output, lipid metabolism, and β-cell compensation. Type 2 diabetes develops through interacting defects in insulin resistance, β-cell dysfunction, adipose inflammation, hepatic glucose overproduction, altered incretin signaling, and ectopic lipid metabolism. A major unresolved question is whether endocrine dysfunction is driven primarily by target-tissue insulin resistance, intrinsic β-cell failure, immune/inflammatory stress, or combined multi-organ failure that differs by disease stage.
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Human Islet Cell Culture
The method of preserving islets in vitro, with purified reduced immunogenicity. The steps are islet isolation, islet cell purification, in vitro determination of islet function and islet cell culture.
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Phalloidin F-actin cytoskeleton staining
Phalloidin F-actin staining detects polymerized filamentous actin in fixed and permeabilized specimens by using fluorescent phalloidin or phalloidin-derived phallotoxins that bind actin filaments and generate a fluorescence microscopy readout corresponding to F-actin organization, including stress fibers, cortical actin, filament bundles, and tissue-specific actin networks. Phalloidin stabilizes F-actin by reducing actin subunit dissociation from filament ends, and fluorescent phallotoxins were established as tools for visualizing actin-containing structures in eukaryotic cells.
Purity & Documentation
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Data Sheet (277 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Handling Instructions (2659 KB)
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)