at 308

AT-308 is a bio-active chemical.

LJI308 是泛RSK 抑制剂，对 RSK1、RSK2 和 RSK3 的IC50分别为 6、4 和 13 nM。它抑制辐照、EGF 处理和表达 KRAS 突变的细胞中 RSK (T359 S363) 和 YB-1 (S102) 的磷酸化。

ERD-308 induces >95% of ER degradation at concentrations as low as 5 nM in both cell lines (DC50 (concentration causing 50% of protein degradation) of 0.17 nM and 0.43 nM in MCF-7 and T47D ER+ cells, respectively).ERD-308 is a highly potent PROTAC degrade

KAG-308 is an effective selective and orally active agonist of the EP4 receptor (Ki: 2.57 nM and EC50: 17 nM for human EP4 receptor), more selective over EP1, EP2, EP3, and IP receptor. KAG-308 suppresses colitis and promotes histological mucosal healing,

RJS308 是一种环孢菌素 A (cyclosporin A) 的PROTAC降解剂，具有284 nM的DC50。RJS308 抑制HIV-1和HCV的复制，从而展现出抗病毒活性。(Pink: ligand for target proteinCypA ligand-2; Black: linker; Blue: ligand for E3ligaseVHL(S,R,S)-AHPC-Me)

WB-308 is an EGFR inhibitor that acts by decreasing NSCLC cell proliferation and colony formation and causing G2 M arrest and apoptosis.

K 308 is a bioactive chemical.

PSAM (pharmacologically selective actuator module) agonist. Activates PSAML141F-GlyR chimeric ion channels. Inhibits activity of neurons expressing PSAML141F-GlyR in vivo and activates locus coeruleus noradrenergic neurons expressing PSAML141F,Y115F-5-HT3 ion channels. Recommended concentration for use in mice is 5 mg kg or lower. Plasmid vectors for the transfection of cells with PSAML141F-GlyR and PSAML141F,Y115F-5-HT3 are available from Addgene. Lovett-Barron et al (2012) Regulation of neuronal input transformations by tunable dendritic inhibition. Nat.Neurosci. 15 423 PMID:22246433 |Satoh et al (2016) Context-dependent gait choice elicited by EphA4 mutation in Lbx1 spinal interneurons. Neuron 89 1046 PMID:26924434 |Atasoy et al (2012) Deconstruction of a neural circuit for hunger. Nature 488 172 PMID:22801496 |Hirschberg et al (2017) Functional dichotomy in spinal- vs prefrontal-projecting locus coeruleus modules splits descending noradrenergic analgesia from ascending aversion and anxiety in rats. Elife 6 e29808 PMID:29027903

LG308 是一种新型合成化合物，具有抗微管活性。LG308 诱导细胞凋亡和细胞死亡，并且显著抑制肿瘤生长，具有前列腺癌的研究潜力。LG308 诱导有丝分裂阻滞并显着抑制 G2 M 的进程，这与细胞周期蛋白 B1 和有丝分裂标志物 MPM-2 的上调以及 cdc2 的去磷酸化有关。

QC-308 HCl is a novel Heme Oxygenase-1 Inhibitor (HO-1 IC50=0.27μM; HO-2 IC50=0.46μM).

HU-308 是一种合成大麻素类似物，具有高度选择性的CB2受体激动作用。其对CB2受体的亲和力超过对CB1受体的440倍。CB2受体主要存在于免疫细胞中，调节内源性大麻素系统 (ECS) 的免疫抑制效应。HU-308 展示了抗炎、神经保护及调节小胶质细胞功能的生物活性，适用于神经炎症和视网膜疾病的研究。

CC260 is a selective PI5P4Kα and PI5P4Kβ inhibitor with Kis of 40 nM and 30 nM, respectively. CC260 does not inhibit or weakly inhibits other protein kinases, such as Plk1 and RSK2. CC260 can be used for cell energy metabolism, diabetes and cancer research[1]. In cultured C2C12 myotubes, CC260 (20 μM) enhances Insulin-induced Akt phosphorylation at both Thr-308 and Ser-473 but suppresses S6K phosphorylation (Thr-389) by mTORC1[1]. CC260 (2.5 μM, 5 μM, 10 μM, 20 μM) significantly increases phosphorylation of acetyl-CoA carboxylase (ACC) in a dose-dependent manner[1]. CC260 treatment reduces the ability of BT474 cells to survive serum starvation, which could be rescued by expressing the PI5P4Kβ refractory mutant[1]. In BT474 cells, CC260 treatment causes an increase in glycolytic ATP production[1]. [1]. Song Chen, et al. Pharmacological inhibition of PI5P4Kα β disrupts cell energy metabolism and selectively kills p53- tumor cells. Proc Natl Acad Sci U S A. 2021 May 25;118(21):e2002486118.