2. Membrane Transporter/Ion Channel Neuronal Signaling Apoptosis Immunology/Inflammation NF-κB Metabolic Enzyme/Protease
  3. iGluR Apoptosis Reactive Oxygen Species (ROS)
  4. P3LC7LC-P

P3LC7LC-P is a blood-brain barrier-permeable BRAG2 ligand with a KD of 6.14 μM. P3LC7LC-P binds to BRAG2, thereby disrupting its interaction with the GluA2 subunit of the AMPA receptor and inhibiting glutamate-induced GluA2 endocytosis. P3LC7LC-P exerts neuroprotective effects in oxygen-glucose deprivation-induced and glutamate-induced neurotoxicity models, reduces ROS accumulation and inhibits apoptosis, and reduces cerebral infarct size in a rat model of transient middle cerebral artery occlusion. P3LC7LC-P can be used for the research of ischemic stroke.

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

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P3LC7LC-P

P3LC7LC-P Chemical Structure

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P3LC7LC-P Related Antibodies

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Description

P3LC7LC-P is a blood-brain barrier-permeable BRAG2 ligand with a KD of 6.14 μM. P3LC7LC-P binds to BRAG2, thereby disrupting its interaction with the GluA2 subunit of the AMPA receptor and inhibiting glutamate-induced GluA2 endocytosis. P3LC7LC-P exerts neuroprotective effects in oxygen-glucose deprivation-induced and glutamate-induced neurotoxicity models, reduces ROS accumulation and inhibits apoptosis, and reduces cerebral infarct size in a rat model of transient middle cerebral artery occlusion. P3LC7LC-P can be used for the research of ischemic stroke[1].

In Vitro

P3LC7LC-P (10-50 μM; 24 h) shows no cytotoxicity against HT22 cells, and the cell viability remains above 80% at all tested doses, even at concentrations up to 50 μM[1].
P3LC7LC-P (0.1-10 μM; 26 h) dose-dependently protects HT22 cells against glutamate-induced excitotoxicity, and restores cell viability to 91.92% at the concentration of 10 μM[1].
P3LC7LC-P (0.1-10 μM) protects primary cortical neurons from glutamate-induced excitotoxic injury, and restores cell viability to 71.11% at a concentration of 10 μM[1].
P3LC7LC-P (0.1-10 μM) protects primary cortical neurons against OGD/R-induced injury in a dose-dependent manner, and restores cell viability to 90.63% at 10 μM[1].
P3LC7LC-P (10 μM; 26 h) significantly reduces glutamate-induced ROS accumulation in HT22 cells[1].
P3LC7LC-P (10 μM; 26 h) significantly reduces glutamate-induced apoptosis of HT22 cells, decreasing the total apoptosis rate to 9.4%[1].
P3LC7LC-P (10 μM; 26 h) reduces the Bax/Bcl-2 ratio and the expression level of activated caspase-3[1].
P3LC7LC-P (10 μM; 3 h) significantly inhibits glutamate-induced GluA2 endocytosis in primary cortical neurons[1].

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

P3LC7LC-P Related Antibodies

Cell Viability Assay[1]

Cell Line: HT22 cells
Concentration: 0.1, 1 and 10 μM
Incubation Time: 2 h (preincubation); 24 h (glutamate exposure)
Result: Restored cell viability in a dose-dependent manner: viability reached 71.92% at 0.1 μM, 81.92% at 1 μM, and 91.92% at 10 μM.
Exceeded the protective efficacy of the positive control Tat-GluA2-3Y (68.72% viability at 10 μM).

Others (Intracellular Reactive Oxygen Species Inhibition Assay)[1]

Cell Line: HT22 cells exposed to glutamate
Concentration: 10 μM
Incubation Time: 2 h (preincubation); 24 h (glutamate exposure)
Result: Reduced ROS production by approximately 50% relative to the glutamate-only group.
Showed reduced DCFH-DA fluorescence intensity confirmed by flow cytometry quantification.

Apoptosis Analysis[1]

Cell Line: HT22 cells exposed to glutamate
Concentration: 10 μM
Incubation Time: 2 h (preincubation); 24 h (glutamate exposure)
Result: Reduced total HT22 cell apoptosis from 12.3% (glutamate alone) to 9.4%.
Showed efficacy comparable to Tat-GluA2-3Y (8.7% total apoptosis).
Confirmed reduced apoptotic nuclear condensation via Hoechst staining.

Western Blot Analysis[1]

Cell Line: HT22 cells exposed to glutamate
Concentration: 10 μM
Incubation Time: 2 h (preincubation); 24 h (glutamate exposure)
Result: Significantly decreased the Bax/Bcl-2 ratio increased by glutamate alone.
Reduced cleaved caspase-3 activation induced by glutamate.
Showed efficacy comparable to Tat-GluA2-3Y.
Parmacokinetics
Species Dose Route T1/2 Tmax Cmax AUC0-t AUC0-∞ MRT0-t MRT0-∞ Brain-to-Plasma Ratio
Rat[1] 8 mg/kg s.c. 0.452 h 1 h 6930 ng/mL 12100 ng·h/mL 12100 ng·h/mL 1.24 h 1.24 h 21.3 %
Rat[1] 8 mg/kg i.v. 0.589 h 0.0833 h 6290 ng/mL 3250 ng·h/mL 3250 ng·h/mL 0.683 h 0.691 h /
In Vivo

P3LC7LC-P (8 mg/kg; i.p.; single administration) significantly reduces the cerebral infarction volume to 21.00% in a rat transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke[1].

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

Animal Model: Sprague-Dawley (SD) (male)[1]
Dosage: 8 mg/kg
Administration: i.p.; single dose
Result: Reduced cerebral infarct volume to 21.00%, compared to 31.51% in the tMCAO model group.
Molecular Weight

1252.42

Formula

C60H73N11O15S2
Sequence

{Tyr(4-Pentynoic acid)}-Lys-Cys-Gly-Tyr-Asn-Cys-Tyr-Gly (Disulfide bridge: Cys3-Cys7)
Sequence Shortening

{Tyr(4-Pentynoic acid)}-KCGYNCYG (Disulfide bridge: Cys3-Cys7)
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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P3LC7LC-P Related Classifications

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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:

P3LC7LC-PiGluRApoptosisReactive Oxygen Species (ROS)Ionotropic glutamate receptorsCaco-2 cell monolayersGluA2glutamate-induced excitotoxicitytransient middle cerebral artery occlusionischemic strokeoxygen-glucose deprivationBRAG2AMPA receptorsprimary cortical neuronsHT22 cellsInhibitorinhibitorinhibit

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