2. GPCR/G Protein MAPK/ERK Pathway
  3. Ras
  4. AH001

AH001 is a natural product, which binds a cryptic pocket proximate to GDP within RhoA with KD of 73.16 nM and interacts with GDP, stabilizing RhoA’s interaction with its endogenous inhibitor, RhoGDIα. AH001 reduces the downstream MRTFA nuclear translocation and downregulates fibrosis/hypertrophy proteins. AH001 mitigates myocardial remodeling in multiple HF animal models, and in the 3D myocardial tissue model. AH001 exerts its cardioprotective effects through the RhoA-RhoGDIα axis, effectively inhibiting downstream RhoA activation signaling[1].

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AH001 Chemical Structure

AH001 Chemical Structure

CAS No. : 1456769-95-1

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Description

AH001 is a natural product, which binds a cryptic pocket proximate to GDP within RhoA with KD of 73.16 nM and interacts with GDP, stabilizing RhoA’s interaction with its endogenous inhibitor, RhoGDIα. AH001 reduces the downstream MRTFA nuclear translocation and downregulates fibrosis/hypertrophy proteins. AH001 mitigates myocardial remodeling in multiple HF animal models, and in the 3D myocardial tissue model. AH001 exerts its cardioprotective effects through the RhoA-RhoGDIα axis, effectively inhibiting downstream RhoA activation signaling[1].

In Vitro

AH001 (20 μM) reduces levels of RhoA-GTP in HEK 293F cells[1].

AH001 (7.8 nM to 1 μM) shows a concentration-dependent decrease in the RhoA GTP/GDP exchange ratio, with IC50 value of 25.72 nM in HEK 293F cells[1].

AH001 (20 μM) interacts with RhoA-GDP and stabilize the RhoA-RhoGDIα binding to constrain RhoA in the GDP-bound state in HEK 293F cells[1].

AH001 (10-40 μM, 24 h) inhibits the downstream signaling of RhoA activation by reducing the level of RhoA-GTP (20 μM), the F-actin formation, and the nuclear translocation of MRTFA in cardiac fibroblasts and Ang II-induced myocardial hypertrophy (cardiomyocytes isolated from neonatal rats)[1].

AH001 (10-40 μM, 24 h) decreases levels of fibrosis-related proteins in fibroblasts, including FN1, COL3[1].

AH001 (10-40 μM, 24 h) effectively suppresses the proliferation of fibroblasts, thereby significantly alleviating the pathological contraction of cardiomyocytes in a dose dependent manner in the 3D myocardial tissue model[1].

AH001 (20 μM, 24 h) exerts its anti-fibrotic effect in a RhoGDIα-dependent manner, and stabilizes the RhoA-RhoGDIα complex to inhibit fibroblast proliferation and activation, promote cardiomyocyte survival, and block pro-fibrotic MRTFA signaling in the 3D myocardial tissue model[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

AH001 Related Antibodies

Cell Migration Assay [1]

Cell Line: Cardiac fibroblasts
Concentration: 10, 20, and 40 μM
Incubation Time: 24 h
Result: Inhibited the migration of cardiac fibroblasts.

Western Blot Analysis[1]

Cell Line: Cardiac fibroblasts
Concentration: 10, 20, and 40 μM
Incubation Time: 24 h
Result: Decrease the level of RhoA-GTP in cardiac fibroblasts, cardiomyocytes.
Decreased levels of Fibronectin 1 (FN1), Collagen type III (COL3), Serum Response Factor (SRF), Vimentin (VIM), and the phosphorylation of Cofilin (CFN) in fibroblasts.

Immunofluorescence[1]

Cell Line: Cardiac fibroblasts, cardiomyocytes, 3D myocardial tissue model (cardiomyocytes and fibroblasts)
Concentration: 10, 20, and 40 μM
Incubation Time: 24 h
Result: Decrease the level of F-actin formation and nuclear translocation of MRTFA in cardiac fibroblasts and cardiomyocytes.
Acted on RhoA-RhoGDIα axis to inhibit the downstream signaling of RhoA activation in cardiomyocytes.
Reduced the expression levels of α-SMA and Vimentin in the 3D myocardial tissue model.
Decreased colocalization of RhoA and RhoGDIα in the 3D myocardial tissue model.
In Vivo

AH001 alleviates myocardial remodeling in multiple HF animal models[1].

AH001 (15.16-166.64 μM) alleviates myocardial remodeling in ISO-induced myocardial hypertrophy in zebrafish at 2 dpf[1].

AH001 (10 mg/kg, i.g., 4weeks) alleviates myocardial remodeling in Angiotensin II (Ang II)-induced mice (8 weeks) models[1].

AH001 (3-30mg/kg, i.g., 1weeks) alleviates myocardial remodeling in LAD coronary artery ligation models in 8-week-old mice and rats[1].

AH001 (1-50 mg/kg, i.g., 12 days) alleviates myocardial remodeling Dox-induced cardiotoxicity models in 8-week-old mice[1].

AH001 (10 mg/kg, i.g., 1weeks) exerts its cardioprotective effects through the RhoA-RhoGDIα axis, effectively inhibiting downstream RhoA activation signaling in LAD mice[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Isopropyl hyperglandrin (ISO)-induced cardiomyocyte hypertrophy models in zebrafish at 2 dpf[1].
Dosage: 15.16, 50.49, 166.64 μM
Administration: In the minimum for 3days
Result: Improved the ISO-induced myocardial hypertrophy, the ejection fraction (EF), the fractional shortening (FS), the blood flow rate, ventricular area, and cardiomyocyte area in zebrafishes with the minimum dose of 15.16 μM, which is comparable to LCZ696 at the dose of 69.59 μM.
Animal Model: Angiotensin II (Ang II)-induced models in 8-week-old mice[1].
Dosage: 10 mg/kg
Administration: Oral gavage for 4 weeks
Result: Improved cardiac functions comparable to the mice treated with LCZ696 at 66.67 mg/kg, assessed by echocardiography, Masson’s trichrome staining, and wheat germ agglutinin (WGA) staining.
Elevated EF and FS, reduced fibrosis areas, and decreased cardiomyocyte areas.
Restored the systolic blood pressure (SBP) and the diastolic blood pressure (DBP) to normal levels.
Animal Model: Left anterior descending (LAD) coronary artery ligation models in 8-week-old mice and rats[1].
Dosage: 3, 10, 30 mg/kg
Administration: Oral gavage for 1 week
Result: Improved cardiac functions at the minimum dose of 3 mg/kg, which is comparable to LCZ696 (66.67 mg/kg) in mice.
Reduced levels of NT-proBNP, lactate dehydrogenase (LDH), creatine kinase (CK), and Ang II in mice.
Reversed the upregulation expression of Rhoa, Postn, Acta2, and Runx1, Spp1 (Osteopontin, OPN) in mice (scRNA-seq) at 10 mg/kg.
Downregulated expression of Rhoa and Nppa (Precursor of ANP, a marker for HF) in mice (scRNA-seq) at 10 mg/kg.
Exhibited moderate Mrtfa expression levels in approximately 20% of cardiomyocytes in mice (scRNA-seq) at 10 mg/kg.
Reduced the levels of NT-proBNP, LDH, CK, and BNP in rats.
Animal Model: Doxorubicin (Dox)-induced cardiotoxicity models in 8-week-old mice[1].
Dosage: 1, 10, 50 mg/kg
Administration: Oral gavage for 12 days
Result: Significantly improved cardiac functions and the extent of myocardial injury.
Improved cardiac vacuole index and fibrosis in the heart (H&E staining and Sirius red staining).
Animal Model: LAD models in myocardium-specific RhoGDIα knockout mice[1].
Dosage: 10 mg/kg.
Administration: Oral gavage for 1 week
Result: Genetic ablation of RhoGDIα substantially attenuated the therapeutic effects of AH001, as evidenced by impaired recovery of cardiac function indicators, persistent fibrotic remodeling, unaltered myocardial hypertrophy, and no significant improvement in fibrosis areas or cardiomyocyte areas.
Molecular Weight

166.22

Formula

C10H14O2
CAS No.
SMILES

CCC1=CC=CC([C@@H](O)CO)=C1
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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

AH0011456769-95-1AH 001AH-001RasHeart failureRhoAGTPasesRhoA-GTPRhoA-RhoGDIαNatural productCardiac fibroblasts.Inhibitorinhibitorinhibit

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