2. Metabolic Enzyme/Protease Vitamin D Related/Nuclear Receptor Immunology/Inflammation Stem Cell/Wnt Apoptosis
  3. Phosphodiesterase (PDE) Glucocorticoid Receptor Wnt β-catenin Apoptosis
  4. Mirodenafil dihydrochloride

Mirodenafil dihydrochloride  (Synonyms: SK-3530 dihydrochloride)

Cat. No.: HY-14930A Purity: 99.85%
COA Handling Instructions

Mirodenafil (SK3530) dihydrochloride is an orally active, potent, reversible, and selective phosphodiesterase 5 (PDE5) inhibitor. Mirodenafil dihydrochloride is a glucocorticoid receptor (GR) modulator Mirodenafil dihydrochloride activates the Wnt/β-catenin signaling pathway by downregulating Dkk1 expression. Mirodenafil dihydrochloride can be used for the research of erectile dysfunction (ED), Alzheimer’s disease (AD) and systemic sclerosis (SSc).

For research use only. We do not sell to patients.

Mirodenafil dihydrochloride Chemical Structure

Mirodenafil dihydrochloride Chemical Structure

CAS No. : 862189-96-6

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Solid + Solvent
10 mM * 1 mL in DMSO
ready for reconstitution
 USD 74 In-stock
Solution
10 mM * 1 mL in DMSO USD 74 In-stock
Solid
5 mg USD 56 In-stock
10 mg USD 90 In-stock
50 mg USD 270 In-stock
100 mg USD 430 In-stock
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Based on 1 publication(s) in Google Scholar

Other Forms of Mirodenafil dihydrochloride:

Mirodenafil dihydrochloride Related Antibodies

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  • Purity & Documentation

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Description

Mirodenafil (SK3530) dihydrochloride is an orally active, potent, reversible, and selective phosphodiesterase 5 (PDE5) inhibitor. Mirodenafil dihydrochloride is a glucocorticoid receptor (GR) modulator Mirodenafil dihydrochloride activates the Wnt/β-catenin signaling pathway by downregulating Dkk1 expression. Mirodenafil dihydrochloride can be used for the research of erectile dysfunction (ED), Alzheimer’s disease (AD) and systemic sclerosis (SSc)[1][2][3].

IC50 & Target

PDE5

 

In Vitro

Mirodenafil dihydrochloride (0-40 μM, 24 h) exerts neuroprotective functions via activating the cGMP/PKG/CREB signaling pathway[2].
Mirodenafil dihydrochloride (0-40 μM, 24 h) enhances neuronal survival by protecting the mitochondrial membrane potential and inhibiting apoptosis[2].
Mirodenafil dihydrochloride (0-40 μM) inhibits GSK-3β signaling, resulting in reduced tau phosphorylation, decreased Aβ production by inhibiting amyloidogenesis and activating the autophagosomal pathway[2].
Mirodenafil dihydrochloride inhibits the transcriptional activity of the glucocorticoid receptor (GR), and inhibits homodimerization of GR in HT-22 cells[2].
Mirodenafil dihydrochloride (0-100 μM, 24 h) inhibits TGF-β-induced phosphorylation of Smad2/3 and mRNA expression of the fibrosis marker in fibroblasts[3].

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

Mirodenafil dihydrochloride Related Antibodies

Western Blot Analysis[2]

Cell Line: SH-SY5Y human neuroblastoma cells
Concentration: 0, 10, 20, 40 μM
Incubation Time: 24 h
Result: Significantly increased cGMP levels by about 200% in a dose-dependent manner. Reversed the Aβ-induced decrease in phosphorylated CREB in a dose-dependent manner. Aβ42 alone increased the levels of cleaved caspase-3 and cleaved PARP, whereas the combined treatment with mirodenafil markedly reduced the expression levels of both apoptotic markers.

RT-PCR[3]

Cell Line: NIH3T3 mouse embryonic fibroblasts
Concentration: 0, 10, 100 μM
Incubation Time: 24 h
Result: The mRNA expression of COL1A1, α-SMA, and CTGF were induced by treatment with TGF-β1, and Mirodenafil significantly reduced the expression of these profibrotic genes.
In Vivo

Mirodenafil dihydrochloride (4 mg/kg, IP, daily for 4 weeks) enhances the cognitive-behavioral performance in transgenic AD mice[2].
Mirodenafil dihydrochloride (0-10 mg/kg, Orally, daily for 3 weeks) ameliorates dermal fibrosis in a BLM-induced SSc mouse model by inhibiting the TGF-β signaling pathway, thereby suppressing the expression of collagen and profibrotic genes[3].

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

Animal Model: APP-C105 transgenic mice (13-month-old, male, n=6)[2]
Dosage: 4 mg/kg
Administration: IP, daily for 4 weeks
Result: Improved cognitive function in the APP-C105 AD mice.
Animal Model: Male BALB/c mice (8 weeks old, four groups, n=10/group)[3]
Dosage: 0, 5 or 10 mg/kg
Administration: Orally, daily for 3 weeks
Result: Ameliorated dermal fibrosis and downregulated the protein levels of fibrosis markers including COL1A1 and α-SMA in the BLM-induced SSc mouse model. Significantly decreased dermal thickness and collagen content.
Clinical Trial
Molecular Weight

604.59

Appearance

Solid

Formula

C26H39Cl2N5O5S
CAS No.
SMILES

[H]Cl.[H]Cl.O=C1C(N(CC)C=C2CCC)=C2N=C(C3=CC(S(=O)(N4CCN(CCO)CC4)=O)=CC=C3OCCC)N1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Solvent & Solubility
In Vitro: 

DMSO : ≥ 100 mg/mL (165.40 mM)

H2O : 5 mg/mL (8.27 mM; ultrasonic and warming and heat to 60°C)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.6540 mL 8.2701 mL 16.5401 mL
5 mM 0.3308 mL 1.6540 mL 3.3080 mL
10 mM 0.1654 mL 0.8270 mL 1.6540 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.5 mg/mL (4.14 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 2.5 mg/mL (4.14 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% Corn Oil

    Solubility: ≥ 2.5 mg/mL (4.14 mM); Clear solution

*All of the co-solvents are available by MedChemExpress (MCE).
Purity & Documentation
References
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Mirodenafil dihydrochloride Related Classifications

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.

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Keywords:

Mirodenafil862189-96-6SK-3530SK3530SK 3530Phosphodiesterase (PDE)Glucocorticoid ReceptorWntβ-cateninApoptosisBeta cateninerectile dysfunctionEDAlzheimer’s diseasesystemic sclerosisfibrosisNIH3T3MRC-5 cellsSH-SY5YHT-22 cellsInhibitorinhibitorinhibit

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