perk

AMG PERK 44 is an orally active and selective PERK inhibitor (IC50: 6 nM) that induces autophagy. It also inhibits GCN2 (IC50: 7300 nM) and B-Raf (IC50 >1000 nM), making it useful for cancer research.

PERK-IN-6 is a novel and highly potent PERK inhibitor (IC50:2.5 nM).

GCN2-IN-6 is also a eIF2α kinase PERK inhibitor with an IC50 of 0.26 nM (in enzymatic assay) and 230 nM (in cells). GCN2-IN-6  is a potent, and orally available GCN2 inhibitor confirmed by in-house enzymatic (IC50 of 1.8 nM) and cellular assays (IC50 of 9

GP 1a is a potent agonist of cannabinoid receptor 2 (CB2) (EC50=7.1), as shown in cAMP, GTPγS and β-arrestin recruitment assays. GP 1a is approximately 30-fold more selective for CB2 receptors than CB1 receptors and increases P-ERK1/2 expression in HL-60 cells in vitro. GP 1a is beneficial for skin wound healing. GP 1a inhibits inflammation and fibrogenesis while promoting epithelial re-formation.

GSK2656157 is a highly specific and ATP-competitive PERK inhibitor (IC50: 0.9 nM) in a cell-free assay. The selectivty is 500-fold higher against a panel of 300 kinases.

ISRIB is a potent and selective PERK inhibitor.

GSK2606414 is a cell-permeable and orally active protein kinase R-like endoplasmic reticulum kinase(PERK)inhibitor with IC50 of 0.4 nM. GSK2606414 inhibits PERK activation in cells and suppresses the growth of human tumor xenografts in mice.

SHP099 (SHP099 free base) free base is an effective, selective, orally bioavailable, and efficacious SHP2 inhibitor (IC50 =0.07 μM and p-ERK modulation in cells IC50 = 0.250 μM). SHP099 shows dose-dependent pathway inhibition and antitumor activity in xenograft models.

ISRIB (trans-isomer) is a potent inhibitor of PERK (IC50=5 nM) that restores protein translation and prevents SG formation in the presence of P-eIF2α.

MK-28 is a selective PERK agonist that reduces toxicity and prolongs survival in a Huntington's disease model.MK-28 has a significant killing effect on MK28 gastric cancer cells.

PERK-IN-4 is a potent and selective PERK inhibitor with an IC50 value of 0.3 nM, used in the study of cancer and neurological disorders.

MSU-42011 is an orally active retinoid X receptor-like (RXR) agonist. It potently inhibits the expression of iNOS, low SREBP-induced and activated RXR, and p-ERK at the protein level. MSU-42011 has demonstrated antitumor activity in a [kras]-driven mouse model of lung cancer and is effective for the treatment of preclinical [kras]-driven lung cancer with immunomodulatory activity.

BAY 2965501 is a potent and selective diacylglycerol kinase zeta (DGKζ) inhibitor that induces pERK activation, and it can be utilized in cancer research.

ONO-8130 is an orally available antagonist of EP1 receptor.

Takeda-6d, a novel, potent DFG-out RAF/vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor, inhibits B-RAF and VEGFR2 with IC50 of 7.0nM and 2.2nM.

PERK-IN-2 is a potent inhibitor of PERK with an IC50 of 0.2 nM.

PERK-IN-3 is a potent inhibitor of PERK (IC50 of 7.4 nM).

(S)-PERK-IN-5, the S-enantiomer of PERK-IN-5, is a PERK inhibitor with an IC50 range of 0.101-0.250 μM.

PERK-IN-5 is a highly selective, potent, orally active inhibitor of protein kinase R-like endoplasmic reticulum (ER) kinase (PERK), displaying inhibition with IC50 values of 2 nM for PERK and 9 nM for p-eIF2α. PERK-IN-5 significantly inhibited tumor growth in the 786-O renal cell carcinoma xenograft tumor model.

Compound V8 (PERK eIF2α activator 1), a flavonoid, exhibits anti-tumor properties by inducing apoptosis and activating the PERK-eIF2α-ATF4 pathway. It effectively inhibits the proliferation of HepG2 cells, with an IC 50 value of 23 μM [1].

Piperkadsin A effectively inhibits reactive oxygen species (ROS) production, specifically targeting PMA-induced ROS in human polymorphonuclear neutrophils, exhibiting an inhibition concentration (IC50) of 4.3 μM [1].

Rocaglamide (Roc-A), isolated from the genus Aglaia, can be used to treat coughs, injuries, asthma, and inflammatory skin diseases. It is a potent inhibitor of NF-κB activation in T-cells.

CCT020312 (0-9 µM, 24 h) treatment of medium HT29 cells for 24 h resulted in a concentration-dependent loss of P-S608-pRB signaling with linear response values between 1.8 and 6.1 µM.

ATPγS tetralithium salt is a good substrate for RNA-stimulated nucleotide hydrolysis and RNA unwinding activity of eIF4A.