JD03-02
JD03-02 is an orally active, blood-brain barrier-permeable TRPC1/5 heterodimer inhibitor with an IC50 of 0.2 nM. JD03-02 preferentially binds to a unique ligand-binding pocket at the interface of TRPC1-TRPC5, exerts almost no inhibitory effect on TRPC5 homotetramers, and thus avoids side effects such as obesity and hyperkinesia. JD03-02 induces anxiolytic and antidepressant effects in mouse models. JD03-02 can be used in studies related to depression and anxiety disorders.
For research use only. We do not sell to patients.
- Formula: C25H27Cl2N5O3
- Molecular Weight:516.42
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
IC50 & Target
[1]|
TRPC1/5 0.2 nM (IC50) |
TRPC1/4 6.7 nM (IC50) |
TRPC5 8504 nM (IC50) |
TRPC4 2385 nM (IC50) |
In Vitro
JD03-02 (10 μM) potently inhibits TRPC1/5 heteromer-mediated calcium influx in HEK293T cells, whereas it exerts no effect on TRPC5 homomers at the concentration of 10 μM[1].
JD03-02 potently inhibits TRPC1/5 heteromers in HEK293T cells with an IC50 of 0.2 nM, and exhibits over 10000-fold selectivity over TRPC5 homomers (IC50 = 8504 nM)[1].
JD03-02 inhibits TRPC1/4 heteromers in HEK293T cells with an IC50 of 6.7 nM, and exhibits selectivity for TRPC4 homomers (IC50 = 2385 nM)[1].
JD03-02 (10 μM) exhibits only extremely low activity against human TRPC3, TRPC6 and TRPC7, with an inhibition rate of no more than 40% at a concentration of 10 μM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
JD03-02 (3-30 mg/kg; p.o.; single administration) exerts dose-dependent anxiolytic effects in mCPP (HY-101324)-induced anxiety-like mice[1].
JD03-02 (10 mg/kg; p.o.; once daily; 11 days) does not induce weight gain or hyperphagia in diet-induced obese mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (male, 7-8 weeks old, chronic unpredictable mild stress-induced depression model)[1]
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Dosage:3 mg/kg; 10 mg/kg; 30 mg/kg (single dose; daily for 14 days)
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Administration:p.o.; daily (14 days); single dose
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Result:Significantly increased sucrose preference compared to vehicle control after a single 30 mg/kg dose.
Significantly increased sucrose preference compared to vehicle control after 11 days of daily treatment with 3 mg/kg, 10 mg/kg, and 30 mg/kg doses, with the 30 mg/kg dose showing greater improvement than the 3 mg/kg dose.
Significantly reduced immobility time in the forced swim test compared to vehicle control after 14 days of daily treatment with 3 mg/kg, 10 mg/kg, and 30 mg/kg doses, with the 30 mg/kg dose showing greater improvement than the 3 mg/kg dose.
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Animal Model:C57BL/6J (male, 7-8 weeks old, mCPP-induced anxiety model)[1]
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Dosage:3 mg/kg; 10 mg/kg; 30 mg/kg
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Administration:p.o.; single dose
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Result:Dose-dependently increased open arm entries and time spent in open arms in the elevated plus maze compared to vehicle control.
Dose-dependently reduced the number of marbles buried in the marble burying test compared to vehicle control.
Dose-dependently increased central zone entries and time spent in the central zone in the open field test compared to vehicle control.
Showed significantly superior efficacy to diazepam in the open field test at 30 mg/kg.
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Animal Model:C57BL/6J (male, 14 weeks old, high-fat diet-induced obesity model)[1]
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Dosage:10 mg/kg
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Administration:p.o.; daily; 11 days
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Result:Had no significant effect on body weight compared to vehicle control.
Had no significant effect on daily or cumulative food intake compared to vehicle control.
Chemical Information
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Molecular Weight 516.42
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Formula C25H27Cl2N5O3
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SMILES
CN(CCCCN1C(C2=C(N(C1=O)C)N=C(N2CC3=CC=C(C=C3)Cl)OC4=CC=CC(Cl)=C4)=O)C
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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.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Metabolic Diseases
AMP-activated protein kinase, AMPK, is a conserved cellular energy sensor that responds to reduced cellular energy status and coordinates metabolism by increasing ATP-generating catabolic pathways while suppressing ATP-consuming anabolic processes. In metabolic disease research, the AMPK pathway is experimentally relevant because it regulates hepatic lipid synthesis, fatty acid oxidation, glucose production, skeletal-muscle glucose disposal, mTORC1-linked biosynthesis, autophagy, mitochondrial homeostasis, and whole-body energy balance. The central pathway logic is that energy stress, metformin, exercise-like stimulation, or direct AMPK activators increase AMPKα Thr172 phosphorylation and downstream substrate phosphorylation, including ACC and RAPTOR. Phosphorylation of ACC suppresses lipogenesis and supports fatty acid oxidation, whereas phosphorylation of RAPTOR suppresses mTORC1 signaling and links cellular energy status to growth and protein synthesis control. The pathway is linked
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
JD03-02 Related Classifications
HY-184164 Related Classifications
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