ITX5061 free base
Based on 3 publication(s) in Google Scholar
ITX5061 free base is an orally active type II non-competitive p38 MAPK inhibitor. ITX5061 free base increases HDL-C levels by inhibiting SR-BI activity. ITX5061 free base also moderately elevates ApoA-I levels. ITX5061 free base reduces early atherosclerotic lesions in the aortic arch of mice fed an atherogenic diet. ITX5061 free base can be used in the research of atherosclerosis.
For research use only. We do not sell to patients.
- CAS No.: 848144-15-0
- Formula: C30H37N3O7S
- Molecular Weight:583.70
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Publications Citing Use of MedChemExpress (MCE) ITX5061 free base
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| CHO | IC50 |
0.77 μM
Compound: ITX-5061
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Inhibition of mouse SR-BI isoform 1 expressed in CHO cells assessed as reduction in uptake of [3H]CE from [3H]CE-HDL by by liquid scintillation counting method
Inhibition of mouse SR-BI isoform 1 expressed in CHO cells assessed as reduction in uptake of [3H]CE from [3H]CE-HDL by by liquid scintillation counting method
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[PMID: 25958245] |
In Vitro
ITX5061 (1 μM) free base significantly inhibits SR-BI-mediated HDL uptake in HEK 293 cells overexpressing SR-BI[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
ITX5061 (30 mg/kg; daily; 7 days) free base increases HDL-C levels in WT mice in an SR-BI-dependent manner, with no effect on HDL-C in SR-BI−/− mice[1].
ITX5061 (0.037% incorporated into diet; daily; 18 weeks) free base increases HDL-C by 30% and reduces early atherosclerotic lesions in the aortic arch by 40% in Ldlr+/− mice fed a Paigen diet for 18 weeks, regardless of CETP expression[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57Bl/6 human apoA-I transgenic (HuAITg)[1]
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Dosage:30 mg/kg
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Administration:daily; 7 days
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Result:Increased HDL-C levels by 50% compared to baseline.
Did not change non-HDL-C levels.
Increased apoA-I levels by 15% compared to vehicle controls.
Induced a shift towards larger-sized HDL.
Decreased HDL-CE fractional catabolic rate to 1.86 pools/d (vs 2.47 pools/d in controls, P<0.05).
Kept HDL-CE production rates identical to controls at 129 μg/g/d.
Reduced accumulation of [3H] CE in the liver significantly.
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Animal Model:F1 hybrid C57BL/6 × DBA/1 Ldlr+/− (with or without CETP expression induced by AAV-CETP injection; fed Paigen high-fat/cholesterol/bile salt diet for 18 weeks)[1]
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Dosage:0.037% incorporated into diet
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Administration:daily; 18 weeks
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Result:Increased HDL-C concentrations by 30%.
Showed no differences in total cholesterol or triglyceride levels compared to controls.
Reduced early atherosclerotic lesions in the aortic arch by 40% (both with and without CETP expression).
Showed a non-significant trend towards reduced lesion area in the aortic valves.
Chemical Information
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CAS No. 848144-15-0
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Molecular Weight 583.70
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Formula C30H37N3O7S
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SMILES
O=C(NC=1C=C(C=C(NS(=O)(=O)C)C1OC)C(C)(C)C)C(=O)C2=CC=C(OCCN3CCOCC3)C=4C=CC=CC24
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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 (3)
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Journal Impact Factor
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Most Recent
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Nat Metab
2020 Dec;2(12):1391-1400. PMID: 33244168 -
iScience
The HDL-transporting scavenger receptor B1 promotes viral infection through endolysosomal acidification. [Abstract]2025 Apr 24;28(6):112501. PMID: 40475258 -
Protocols
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
ITX5061 free base Related Classifications
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