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Catalog No.: GC32209

ITX5061 is a type II inhibitor of p38 MAPK and also an antagonist of scavenger receptor B1 (SR-B1).

ITX5061 Chemical Structure

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5 mg
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10 mg
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50 mg
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Animal experiment:

Atherosclerosis studies are conducted in F1 hybrid C57BL/6×DBA/1 Ldlr+/- mice fed the Paigen diet, which is high-fat/cholesterol/bile salt diet containing 1.25% cholesterol, 7.5% cocoa butter, and 0.5% cholic acid. For 18 weeks, the mice are put on the Paigen diet with or without ITX5061 at 0.037 %. CETP expression is induced by injection of adeno-associated virus (AAV)8 TBG human CETP vector two weeks before starting the Paigen diet. Doses of virus are given by IP injection[1].


[1]. Masson D, et al. Increased HDL cholesterol and apoA-I in humans and mice treated with a novel SR-BI inhibitor. Arterioscler Thromb Vasc Biol. 2009 Dec;29(12):2054-60.


ITX5061 is a type II inhibitor of p38 MAPK and also an antagonist of scavenger receptor B1 (SR-B1).

ITX5061 is a type II inhibitor of p38 MAPK and also an antagonist of scavenger receptor B1 (SR-B1). Treatment of ITX5061 (30 mg/kg/day) for mice results in a 50% increase in HDL-C levels compare to baseline. ApoA-I levels are moderately (+15 %) but significantly increased in ITX5061-treated HuAITg mice, compare to mice receive vehicle. ITX5061 significantly decreases HDL-CE catabolism with an FCR of 1.86±0.40 pools/d vs 2.47±0.26 pools/d in the control group (P<0.05), while calculated production rates are identical in both groups (129±24 μg/g/d vs 129±16 μg/g/d). Moreover, accumulation of [3H] CE in the liver is significantly lower in ITX5061-treated mice indicating that increased HDL-CE levels are due to reduced uptake by the liver[1].

[1]. Masson D, et al. Increased HDL cholesterol and apoA-I in humans and mice treated with a novel SR-BI inhibitor. Arterioscler Thromb Vasc Biol. 2009 Dec;29(12):2054-60.

Chemical Properties

Cas No. 1252679-52-9 SDF
Canonical SMILES O=C(NC1=CC(C(C)(C)C)=CC(NS(=O)(C)=O)=C1OC)C(C2=C3C=CC=CC3=C(OCCN4CCOCC4)C=C2)=O.Cl
Formula C30H38ClN3O7S M.Wt 620.16
Solubility DMSO : ≥ 83.3 mg/mL (134.32 mM) Storage Store at -20°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request

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Research Update

Effect of scavenger receptor class B type I antagonist ITX5061 in patients with hepatitis C virus infection undergoing liver transplantation

Liver Transpl 2016 Mar;22(3):287-97.PMID:26437376DOI:10.1002/lt.24349.

Hepatitis C virus (HCV) entry inhibitors have been hypothesized to prevent infection of the liver after transplantation. ITX5061 is a scavenger receptor class B type I antagonist that blocks HCV entry and infection in vitro. We assessed the safety and efficacy of ITX5061 to limit HCV infection of the graft. The study included 23 HCV-infected patients undergoing liver transplantation. The first 13 "control" patients did not receive drug. The subsequent 10 patients received 150 mg of ITX5061 immediately before and after transplant and daily for 1 week thereafter. ITX5061 pharmacokinetics and plasma HCV RNA were quantified. Viral genetic diversity was measured by ultradeep pyrosequencing (UDPS). ITX5061 was well tolerated with measurable plasma concentrations during therapy. Although the median HCV RNA reduction was greater in ITX-treated patients at all time points in the first week after transplantation, there was no difference in the overall change in the area over the HCV RNA curve in the 7-day treatment period. However, in genotype (GT) 1-infected patients, treatment was associated with a sustained reduction in HCV RNA levels compared to the control group (area over the HCV RNA curve analysis, P = 0.004). UDPS revealed a complex and evolving pattern of HCV variants infecting the graft during the first week. ITX5061 significantly limited viral evolution where the median divergence between day 0 and day 7 was 3.5% in the control group compared to 0.1% in the treated group. In conclusion, ITX5061 reduces plasma HCV RNA after transplant notably in GT 1-infected patients and slows viral evolution. Following liver transplantation, the likely contribution of extrahepatic reservoirs of HCV necessitates combining entry inhibitors such as ITX5061 with inhibitors of replication in future studies.

Safety and antiviral activity of the HCV entry inhibitor ITX5061 in treatment-naive HCV-infected adults: a randomized, double-blind, phase 1b study

J Infect Dis 2014 Mar 1;209(5):658-67.PMID:24041792DOI:10.1093/infdis/jit503.

Background: Hepatitis C virus (HCV) entry involves scavenger receptor B1 (SRB1). In vitro, SRB1 inhibition by ITX5061 impedes HCV replication. Methods: Multicenter study to assess safety/activity of ITX5061 in previously untreated, noncirrhotic, HCV genotype 1 infected adults. Design included sequential cohorts of 10 subjects with ITX5061 (n = 8) or placebo (n = 2) to escalate duration (3 to 14 to 28 days) or deescalate dose (150 to 75 to 25 mg) based on predefined criteria for safety and activity (鈮?4 of 8 subjects with HCV RNA decline 鈮?1 log10 IU/mL). Results: Thirty subjects enrolled in 3 cohorts: ITX5061 150 mg/day by mouth for 3 (A150), 14 (B150), and 28 (C150) days. Six subjects had grade 鈮?3 adverse events (one in placebo); none were treatment related. One of the 7 C150 subjects (14.3%, 95% confidence interval [CI], .7%-55.4%) had 鈮?1 log10 IU/mL decline in HCV RNA (1.49 log10 IU/mL), whereas none of the 6 placebo, 8 A150 or 8 B150 subjects showed such decline. Conclusions: Oral ITX5061 150 mg/day for up to 28 days was safe and well tolerated. In the 28-day cohort, 1 of 7 subjects showed antiviral activity; however, predefined criteria for antiviral activity were not met at the doses and durations studied.

Increased HDL cholesterol and apoA-I in humans and mice treated with a novel SR-BI inhibitor

Arterioscler Thromb Vasc Biol 2009 Dec;29(12):2054-60.PMID:19815817DOI:10.1161/ATVBAHA.109.191320.

Objective: Increasing HDL levels is a potential strategy for the treatment of atherosclerosis. Methods and results: ITX5061, a molecule initially characterized as a p38 MAPK inhibitor, increased HDL-C levels by 20% in a human population of hypertriglyceridemic subjects with low HDL levels. ITX5061 also moderately increased apoA-I but did not affect VLDL/LDL cholesterol or plasma triglyceride concentrations. ITX5061 increased HDL-C in WT and human apoA-I transgenic mice, and kinetic experiments showed that ITX5061 decreased the fractional catabolic rate of HDL-CE and reduced its hepatic uptake. In transfected cells, ITX5061 inhibited SR-BI-dependent uptake of HDL-CE. Moreover, ITX5061 failed to increase HDL-C levels in SR-BI(-/-) mice. To assess effects on atherosclerosis, ITX5061 was given to atherogenic diet-fed Ldlr(+/-) mice with or without CETP expression for 18 weeks. In both the control and CETP-expressing groups, ITX5061-treated mice displayed reductions of early atherosclerotic lesions in the aortic arch -40%, P<0.05), and a nonsignificant trend to reduced lesion area in the proximal aorta. Conclusions: Our data indicate that ITX5061 increases HDL-C levels by inhibition of SR-BI activity. This suggests that pharmacological inhibition of SR-BI has the potential to raise HDL-C and apoA-I levels without adverse effects on VLDL/LDL cholesterol levels in humans.

Sprouty2 loss-induced IL6 drives castration-resistant prostate cancer through scavenger receptor B1

EMBO Mol Med 2018 Apr;10(4):e8347.PMID:29540470DOI:10.15252/emmm.201708347.

Metastatic castration-resistant prostate cancer (mCRPC) is a lethal form of treatment-resistant prostate cancer and poses significant therapeutic challenges. Deregulated receptor tyrosine kinase (RTK) signalling mediated by loss of tumour suppressor Sprouty2 (SPRY2) is associated with treatment resistance. Using pre-clinical human and murine mCRPC models, we show that SPRY2 deficiency leads to an androgen self-sufficient form of CRPC Mechanistically, HER2-IL6 signalling axis enhances the expression of androgen biosynthetic enzyme HSD3B1 and increases SRB1-mediated cholesterol uptake in SPRY2-deficient tumours. Systemically, IL6 elevated the levels of circulating cholesterol by inducing host adipose lipolysis and hepatic cholesterol biosynthesis. SPRY2-deficient CRPC is dependent on cholesterol bioavailability and SRB1-mediated tumoral cholesterol uptake for androgen biosynthesis. Importantly, treatment with ITX5061, a clinically safe SRB1 antagonist, decreased treatment resistance. Our results indicate that cholesterol transport blockade may be effective against SPRY2-deficient CRPC.

MEAN inhibits hepatitis C virus replication by interfering with a polypyrimidine tract-binding protein

J Cell Mol Med 2016 Jul;20(7):1255-65.PMID:26929148DOI:10.1111/jcmm.12798.

MEAN (6-methoxyethylamino-numonafide) is a small molecule compound, and here, we report that it effectively inhibits hepatitis C virus (HCV) infection in an HCV cell culture system using a JC1-Luc chimeric virus, with a 50% effective concentration (EC50) of 2.36 卤 0.29 渭M. Drug combination usage analyses demonstrated that MEAN was synergistic with interferon 伪, ITX5061 and ribavirin. In addition, MEAN effectively inhibits N415D mutant virus and G451R mutant viral infections. Mechanistic studies show that the treatment of HCV-infected hepatocytes with MEAN inhibits HCV replication but not translation. Furthermore, treatment with MEAN significantly reduces polypyrimidine tract-binding protein (PTB) levels and blocks the cytoplasmic redistribution of PTB upon infection. In the host cytoplasm, PTB is directly associated with HCV replication, and the inhibition of HCV replication by MEAN can result in the sequestration of PTB in treated nuclei. Taken together, these results indicate that MEAN is a potential therapeutic candidate for HCV infection, and the targeting of the nucleo-cytoplasmic translocation of the host PTB protein could be a novel strategy to interrupt HCV replication.


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Average Rating: 5 ★★★★★ (Based on Reviews and 24 reference(s) in Google Scholar.)

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