sl1

FOSL1 degrader 1 (4) 作为一种T-5224-PROTAC,能够高效地降解FOSL1 (AP-1)以抑制HNSCC癌干性基因的活性.该化合物通过破坏FOSL1来抑制肿瘤增长,且能有效消除HNSCC肿瘤干细胞.在比较中,FOSL1 degrader 1 (4) 的效力比T-5224高出30至100倍.

(R)-SL18 是一种ANXA3降解剂，能够通过泛素化途径降解ANXA3蛋白。它能够抑制乳腺癌细胞的增殖、迁移、侵袭和克隆形成，并诱导细胞凋亡 (apoptosis)，适用于三阴性乳腺癌的研究。

β-Lapachone (ARQ-501) 是一种萘醌类天然产物，是拓扑异构酶 I 抑制剂，通过抑制细胞周期进程来诱导细胞凋亡。

KSL-128114是一种对膜调节剂syntenin的肽抑制剂（Ki = 300 nM）。它能够依赖浓度降低A2058黑色素瘤和患者来源的多形性胶质母细胞瘤（GBM）细胞的存活率。在使用患者来源的GBM细胞并在颅内植入前用KSL-128114培养的患者衍生异种移植（PDX）小鼠模型中，KSL-128114（50 µM）提高了动物的存活时间。

SL-164 是一种喹唑啉酮类化合物，具有镇静作用。

HG6-64-1 is a potent and selective inhibitor of B-Raf (IC50: 0.09 μM on B-raf V600E transformed Ba F3 cells).

TLR2 6 agonist (also a putative TLR10 ligand). Activates NF-κB. Induces pro-inflammatory cytokines including IL-8, IL-1β, CCL20 and TNF-α in vitro. Synergizes with IFNγ to induce CXCL10 release from melanoma cells.

FSL-1 TFA, a bacterial-derived toll-like receptor 2 6 (TLR2 6) agonist, enhances resistance to experimental HSV-2 infection[1]. FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB AP-1 signaling pathways in monocytic THP-1 cells[2]. FSL-1 significantly reduces HSV-2 replication in human vaginal epithelial cells (EC)[1].FSL-1 induces significant resistance to experimental genital HSV-2 infection through elaboration of a specific cytokine response profile[1].FSL-1 (50 ng mL, 24 hours) induces MMP-9 expression at both mRNA and protein levels in human monocytic THP-1 cells[2].FSL-1 activates the MAP kinase NF-κB signaling pathway[2]. Cell Viability Assay[1] Cell Line: V11I, V12I or V19I immortalized human vaginal EC FSL-1 application significantly protectes against genital HSV-2 challenge in mice[1]. Animal Model: Female Swiss-Webster mice (weighing 20-25 g)[1] [1]. William A Rose 2nd, et al. FSL-1, a bacterial-derived toll-like receptor 2 6 agonist, enhances resistance to experimental HSV-2 infection. Virol J. 2009 Nov 10;6:195. [2]. Cathryn J Kurkjian,et al. The Toll-Like Receptor 2 6 Agonist, FSL-1 Lipopeptide, Therapeutically Mitigates Acute Radiation Syndrome. Sci Rep. 2017 Dec 11;7(1):17355.