| Field | Specification |
|---|---|
| Target | |
| Alternative names | LY303070 |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C19H20N4O3 |
| SMILES | |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
GYKI 53784, also known as LY303070, is an orally active, blood-brain-penetrant, selective, non-competitive AMPA receptor antagonist (IC50 0.32 μM) that fully blocks AMPA-mediated synaptic transmission, protects against excitotoxicity, and partially inhibits kainate (kainic acid) responses, indicating activity at both AMPA and kainate receptors. It also selectively blocks synaptic transmission (IC50 365.3 nM) without affecting neuronal excitability and produces potent, stereoselective antinociceptive effects through an opioid-independent mechanism. As a versatile tool for studying AMPA receptor function in synaptic transmission, excitotoxicity, neuroprotection, pain and inflammation, it has potential relevance to hearing loss, neonatal ischemia, neurodegenerative disorders, schizophrenia and Alzheimer's disease[1][2][3][4][5][6][7][8][9][10]. It has the molecular formula C19H20N4O3 and a molecular weight of 352.39 g/mol.
Physical & Chemical Properties
| CAS Number | 161832-71-9 |
|---|---|
| Molecular Formula | C19H20N4O3 |
| Molecular Weight | 352.39 g/mol |
| SMILES | CNC(N1N=C(C2=CC=C(C=C2)N)C3=C(C[C@H]1C)C=C4C(OCO4)=C3)=O |
| Target | AMPA Receptor |
| Signaling Pathway | Membrane Transporter/Ion Channel; Neuronal Signaling |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Biological Activity
IC50 & Target
[1][2][3][4][5][6][7][8][9][10]
|
AMPA Receptor 0.32 μM (IC50) |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with your institution's chemical hygiene plan.
In Vitro
GYKI 53784 (10 mM; 23-120 nA), applied microionophoretically, blocks kainate-induced depolarization (AMPA-mediated under ketamine-diazepam alone); pentobarbitone reverses this block and confers AMPA-versus-kainate selectivity, and both effects need continuous pentobarbitone and reverse on washout[1]. Perfusion of GYKI 53784 (0.1-160 μM; 10 min) selectively blocks AMPA-mediated auditory nerve transmission (hair cell-sparing), while NMDA does not mediate fast cochlear signaling[2]. With perfusion of GYKI 53784 (10-100 μM; 10 min), the sensitivity of auditory nerve fibers correlates with postsynaptic AMPA receptor density, and AMPA/kainate-induced cochlear excitotoxicity is blocked[2]. Perfused GYKI 53784 (50 μM; 20 min) also blocks AMPA/kainate-induced cochlear excitotoxicity[2]. Through AMPA receptor antagonism, GYKI 53784 (50 μM; perfusion; 20 min) blocks Eticlopride-induced excitotoxicity, confirming that loss of dopaminergic inhibition triggers AMPA-mediated dendritic damage[3]. In cultured rat cortical neurons, AMPA receptor-mediated synaptic transmission is selectively blocked by GYKI 53784 (LY303070) (10 μM; IC50 = 365.3 nM), without any effect on direct neuronal excitability[4]. In cerebellar granule neurons, GYKI 53784 (10 μM) effectively isolates kainate receptor-mediated currents by blocking nearly all of the AMPA receptor component while kainate receptor function is preserved[5]. In rat cerebellar Purkinje cells, GYKI 53784 (0.01-10 μM) inhibits the AMPA-induced steady-state current in a concentration-dependent manner, with an IC50 of 0.32 μM[6]. AMPA-induced 3H-GABA release is inhibited non-competitively by GYKI 53784 (0.01 mM)[7]. In brainstem motoneurons, GYKI 53784 (5-20 μM) completely blocks AMPA-mediated synaptic transmission but suppresses kainate responses only partially[9].
In Vivo
In Sprague–Dawley rats, the passive/active membrane electrical properties of motoneurons are not directly affected by GYKI 53784 (LY303070) (2.3 mg/kg; i.v.; single dose); its inhibitory effect is specific to AMPA receptor-mediated excitatory synaptic transmission[1]. In neonatal rats, significant neuroprotective effects against AMPA-induced striatal damage are exerted by GYKI 53784 (2 mg/kg; i.p.; every one hour; for 4 times), which also effectively suppresses AMPA-induced turning behavior and seizure-like activity[8]. Chemical visceral pain is potently suppressed, in a stereospecific manner, by GYKI 53784 (0.01-30 mg/kg; p.o.; single dose)[10]. In the rat tail flick test, GYKI 53784 (0.003-3 mg/kg; p.o.; single dose) shows potent, stereospecific antinociceptive effects[10]. In SPRD rats, GYKI 53784 (0.01 mg/kg; p.o.; single dose) gives no significant synergy with morphine, and Naloxone does not antagonize its antinociceptive effect, indicating that opioid receptor mechanisms are not involved in its action[10]. In SPRD rats, moderate anti-inflammatory effects at high doses are seen with GYKI 53784 (1-10 mg/kg; p.o.; single dose)[10]. In the mouse Zymosan (Zymosan A)-induced paw edema model, GYKI 53784 (10 mg/kg; p.o.; single dose) exhibits anti-inflammatory effects[10].
| Animal Model | Adult Sprague–Dawley rats weighing 220-300 g[1] |
|---|---|
| Dosage | 2.3 mg/kg |
| Administration | i.v., single dose |
| Result | Exerted no significant effect on intrinsic membrane properties of abducens motoneurons. Reversibly depressed trigeminal-evoked EPSPs following intravenous administration. |
| Animal Model | 7-day-old neonatal SPRD breed rats weighing 16-21 g[8] |
|---|---|
| Dosage | 2 mg/kg |
| Administration | i.p.; every one hour; for 4 times |
| Result | Significantly inhibited AMPA-induced abnormal rotational movements and seizure-like seizures in newborn rats. Reduced AMPA-induced striatal tissue damage. |
| Animal Model | Male mice of the CD1 strain weighing 20-25 g[10] |
|---|---|
| Dosage | 0.01-30 mg/kg |
| Administration | p.o., single dose |
| Result | Dose-dependently suppressed phenylquinone-induced writhing, with an ED50 of 0.51 mg/kg. |
| Animal Model | SPRD (Sprague-Dawley) rats weighing 150-200 g[10] |
|---|---|
| Dosage | 0.003 mg/kg, 0.3 mg/kg, 3 mg/kg |
| Administration | p.o., single dose |
| Result | Dose-dependently prolonged tail flick latency, with peak effect at 15 min post-administration and an ED50 of 0.02 mg/kg. |
| Animal Model | SPRD (Sprague-Dawley) rats weighing 150-200 g[10] |
|---|---|
| Dosage | 0.01 mg/kg combined with increasing doses of morphine |
| Administration | p.o.,combined with morphine (s.c.), single dose |
| Result | Had no significant effect on the ED50 of morphine. |
| Animal Model | SPRD (Sprague-Dawley) rats weighing 150-200 g[10] |
|---|---|
| Dosage | 1-10 mg/kg |
| Administration | p.o., single dose |
| Result | Significantly (though moderately) inhibited Carrageenan (λ-Carrageenan)-induced paw edema (max ~25-30%), peaking at 2-3 h after injection. |
| Animal Model | Male mice of the CD1 strain weighing 20-25 g[10] |
|---|---|
| Dosage | 10 mg/kg |
| Administration | p.o., single dose |
| Result | Significantly inhibited zymosan-induced paw edema. |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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