GLyT2-IN-3
GLyT2-IN-3 is a potent GlyT2 inhibitor with a KD of 23.7 nM. GLyT2-IN-3 inhibits GlyT2-mediated glycine uptake with an IC50 of 19.4 nM. GLyT2-IN-3 shows broad-spectrum antinociceptive effects in three pain models, does not induce sedative effects or motor coordination impairment in mice, and exhibits favorable pharmacokinetic properties in rats with an oral bioavailability of 88.57%, GLyT2-IN-3 can be used for the study of neuropathic pain.
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- CAS No.: 2789716-24-9
- Formule: C23H31N3O4
- Masse moléculaire:413.51
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Activité biologique
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Activité biologique
Description
IC50 & Target
[1]|
GlyT2 23.7 nM (Kd) |
In Vitro
GLyT2-IN-3 (compound 14) binds to GlyT2 with a KD of 23.7 nM, a ka of 13.5 × 103 M-1s-1 and a kd of 3.20 × 10-4 s-1[1].
GLyT2-IN-3 shows a distinct binding pose in the GlyT1 pocket compared to the selective GlyT1 inhibitor SSR504734 (HY-10715) in molecular docking[1].
GLyT2-IN-3 (0-10000 nM; 30 min preincubation; 30 min uptake) inhibits GlyT2-mediated 3H-glycine uptake in HEK293 cells stably expressing human GlyT2 with an IC50 of 19.4 nM[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Parmacokinetics
In Vivo
GLyT2-IN-3 (10, 20, 30 mg/kg; s.c.; single dose) in Paclitaxel (HY-B0015)-induced neuropathic pain ICR mice dose-dependently reverses mechanical allodynia, with an ED50 of 12.17 mg/kg[1].
GLyT2-IN-3 (25 mg/kg; s.c.; single dose) in ICR mice produces a 61% inhibition rate in the acetic acid-induced writhing test[1].
GLyT2-IN-3 (36 mg/kg; s.c.; single dose, three times the ED50 in the paclitaxel-induced CIPN model) does not change locomotor activity in the open-field test compared with the vehicle control, and fails to affect the rotarod fall latency at 30, 60, 90 and 120 min post-administration in ICR mice[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Formalin test (Phase II) in ICR mice (20-32 g, both sexes)[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:s.c.; single dose
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Result:Showed an ED50 of 30.5 mg/kg.
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Animal Model:Acetic acid-induced abdominal constriction test in ICR mice (20-32 g, both sexes)[1]
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Dosage:12.5, 25, 50 mg/kg
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Administration:s.c.; single dose
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Result:Showed an ED50 of 26.0 mg/kg.
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Animal Model:Paclitaxel-induced CIPN model in ICR mice (20-32 g, both sexes)[1]
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Dosage:10, 20, 30 mg/kg
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Administration:s.c.; single dose
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Result:Reversed mechanical allodynia with an ED50 of 12.17 mg/kg.
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Animal Model:Strychnine reversal experiment in ICR mice (20-32 g, both sexes)[1]
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Dosage:25 mg/kg
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Administration:s.c.; single dose
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Result:Produced 61% inhibition rate.
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Animal Model:Open-field test in ICR mice (20-32 g, both sexes)[1]
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Dosage:36 mg/kg
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Administration:s.c.; single dose
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Result:Showed no significant alteration in locomotor activity.
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Animal Model:Rotarod test in ICR mice (20-32 g, both sexes)[1]
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Dosage:36 mg/kg
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Administration:s.c.; single dose
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Result:Showed no significant effect on latency to fall.
Chemical Information
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CAS No. 2789716-24-9
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Masse moléculaire 413.51
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Formule C23H31N3O4
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SMILES
O=C(NC1CCN(C2=CC=NC=C2)CC1)C3=CC(OC)=C(OCCCC)C(OC)=C3
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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Protocol for Pharmacokinetic Study
Pharmacokinetic studies quantify how an organism handles a drug over time through absorption, distribution, metabolism, and excretion, and the core experimental readout is the concentration-time profile of parent drug and, when relevant, metabolites in biological matrices such as plasma, whole blood, urine, bile, or tissue. Pharmacokinetic analysis links dose, route, exposure, clearance, half-life, distribution, bioavailability, and systemic exposure to drug efficacy and toxicity hypotheses rather than measuring a signaling pathway directly. The literature links pharmacokinetics to drug-development phenotypes by showing that drug metabolism and pharmacokinetics influence compound progression, exposure-response interpretation, safety margins, dosing strategy, and failure risk during discovery and development. DMPK science contributes to compound optimization by integrating physicochemical properties, in vitro metabolism, transporter behavior, in vivo exposure, and pharmacodynamic contex
Pureté et documentation
Références
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
GLyT2-IN-3 Related Classifications
HY-184901 Related Classifications
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