Jurkat T

Lifitegrast (SAR 1118) 是一种整合素淋巴细胞功能相关抗原 1 拮抗剂， 抑制 Jurkat T 细胞附着于ICAM-1的IC50为 2.98 nM。

NOTA是一种多功能螯合剂，能够与金属离子形成稳定络合物，常用于放射性药物、分子成像和靶向核治疗。

Soquelitinib(CPI-818)是一种共价，不可逆，可口服和选择性的ITK抑制剂, 优先抑制Th2细胞因子的产生而非Th1，抑制小鼠肿瘤的体内生长，并且降低T细胞衰竭标志物，使正常CD8细胞的肿瘤浸润增加和CXCR3、IFNγ、TNFα和CD107a表达上调。

Pheniramine maleate (Trimetose) 是一种具有抗组胺和血管扩张特性的烷基胺衍生物，可与组胺 H1 受体结合，从而抑制磷脂酶 A2 和内皮源性松弛因子一氧化氮的产生。

Tulipalin A (α-methylene-γ-butyrolactone) 是来源于郁金香鳞茎的有毒糖苷。Tulipalin A 是引起过敏性接触皮炎的致敏性致敏物 (causative allergen)，在低剂量影响免疫细胞的功能，例如 Jurkat T 细胞。

2-Nitrobenzoic acid (o-Nitrobenzoic acid) 是一种抗增殖化合物，对表达 T 型钙通道α1H 或其剪接变体δ25的 jurkat 细胞系显示出8.3μM 的 IC50。

Selinexor (KPT-330) 是一种 CRM1 的小分子抑制剂，具有选择性和口服活性。Selinexor 可以阻滞细胞周期、诱导细胞凋亡，具有抗肿瘤活性，可以用于治疗多发性骨髓瘤。

SP-100030 是一种有效的 NF-κB 和激活蛋白-1 (AP-1) 双抑制剂 (IC50 分别为 50 和 50 nM)。SP-10003 抑制 Jurkat 和其他T 细胞系产生的 IL-2、IL-8 和 TNF-α 的产生。SP-100030 降低小鼠胶原性关节炎 (CIA)。

BMS-1001 hydrochloride 是一种人 PD-L1 PD-1免疫检查点的抑制剂，具有口服活性且细胞毒性低。

15-Acetoxyscirpenol, a member of the acetoxyscirpenol moiety mycotoxins (ASMs), potently induces apoptosis and inhibits the growth of Jurkat T cells in a dose-dependent manner. This effect is mediated through the activation of caspases independent of caspase-3[1].

MRK-560 是高效的、口服有效的 γ- 分泌酶抑制剂抑制剂，具有大脑屏障渗透性。

PQA-18 是p21激活激酶2（PAK2；IC50 = 10 nM）的有效抑制剂，并作为Ppc-1（产品编号42352）衍生物展现出免疫抑制特性。该化合物能够降低由刀豆A（产品编号14951）刺激的Jurkat T细胞中IL-2的生成（IC50 = 400 nM）。在应用0.1% PQA-18的情况下，NC Nga小鼠模型显示异位性皮炎的严重程度、血清IgE水平及皮肤厚度有所减轻。此外，0.05%的剂量可有效减少该小鼠模型中皮肤神经纤维的密度。PQA-18（4 mg kg）还在大鼠小肠移植模型中显著提高了移植物的存活率。

HPK1-IN-56 (Compound A29) 是一种HPK1抑制剂，IC50为2.70 nM，抑制下游 p-SLP76 在Jurkat T细胞中的IC50为8.1 nM。此外，HPK1-IN-56 能诱导人PBMCs中IL-2的产生，并表现出抗癌作用，提升T细胞的杀伤能力及增强抗PD-1抗体的抗肿瘤功效。

PD-L1 HDAC6-IN-1 (Compound HP29) 是一种同时抑制PD-L1和HDAC6的化合物，具有抑制PD-L1 PD-1相互作用和HDAC6活性的能力，IC50分别为26.8 nM和69 nM。该化合物增强了Jurkat T细胞对HepG2细胞的杀伤效能，IC50为3.4 μM。在大鼠体内，PD-L1 HDAC6-IN-1展示了良好的药代动力学特征，药物暴露度为871.62 ng·h mL，并且在小鼠B16-F10异种移植模型中表现出抗肿瘤活性。

CTA 056 是白细胞介素-2 诱导的 T 细胞激酶（ITK）抑制剂，抑制小鼠 MOLT-4 异种移植肿瘤的生长，诱导 Jurkat 细胞凋亡，可用于研究自身免疫性疾病和T细胞恶性肿瘤。

Gliovirin is a fungal metabolite that has been found inT. harzianumand has fungicidal, antimicrobial and anti-inflammatory activities.1It is active against the plant pathogenic fungusP. ultimum(MIC = 60 ng/ml) and the parasiteT. brucei brucei(IC50= 90 ng/ml), but has no effect on the plant pathogenic fungiR. solani,P. omnivorum,T. basicola,R. arrhizus, andV. dahliaeor the bacteriaB. thuringiensis,P. fluorescens, andX. malvacearumwhen used at concentrations up to 1,000 ng/ml.2,3Gliovirin decreases phorbol 12-myristate 13-acetate (TPA)- and ionomycin-induced increased expression of COX-2 (IC50= 1 μM) and protein levels of IL-2 in Jurkat cells (IC50= 5.2 μM).1 1.Rether, J., Serwe, A., Anke, T., et al.Inhibition of inducible tumor necrosis factor-α expression by the fungal epipolythiodiketopiperazine gliovirinBiol. Chem.388(6)627-637(2007) 2.Howell, C.R., and Stipanovic, R.D.Gliovirin, a new antibiotic from Gliocladium virens, and its role in the biological control of Pythium ultimumCan. J. Microbiol.29(3)321-324(1983) 3.Iwatsuki, M., Otoguro, K., Ishiyama, A., et al.In vitro antitrypanosomal activity of 12 low-molecular-weight antibiotics and observations of structure/activity relationshipsJ. Antibiot. (Tokyo)63(10)619-622(2010)

HT-2 toxin-13C22is intended for use as an internal standard for the quantification of HT-2 toxin by GC- or LC-MS. HT-2 toxin is a type A trichothecene mycotoxin and an active, deacetylated metabolite of the trichothecene mycotoxin T-2 toxin .1,2Like T-2 toxin, HT-2 toxin inhibits protein synthesis and cell proliferation in plants.2HT-2 toxin also reduces viability of HepG2, A549, HEp-2, Caco-2, A-204, U937, Jurkat, and RPMI-8226 cancer cells with IC50values ranging from 3.1 to 23 ng ml and human umbilical vein endothelial cells with an IC50value of 56.4 ng ml.1It induces oxidative stress, DNA damage, and autophagy in, as well as halts the development of, cultured mouse embryos when used at a concentration of 10 nM.3HT-2 toxin has been found in cereal grains and food products.4,5 1.Nielsen, C., Casteel, M., Didier, A., et al.Trichothecene-induced cytotoxicity on human cell linesMycotoxin Res.25(2)77-84(2009) 2.Nathanail, A.V., Varga, E., Meng-Reiterer, J., et al.Metabolism of the fusarium mycotoxins T-2 toxin and HT-2 toxin in wheatJ. Agric. Food Chem.63(35)7862-7872(2015) 3.Zhang, L., Li, L., Xu, J., et al.HT-2 toxin exposure induces mitochondria dysfunction and DNA damage during mouse early embryo developmentReprod. Toxicol.85104-109(2019) 4.Langseth, W., and Rundberget, T.The occurrence of HT-2 toxin and other trichothecenes in Norwegian cerealsMycopathologia147(3)157-165(1999) 5.Al-Taher, F., Cappozzo, J., Zweigenbaum, J., et al.Detection and quantitation of mycotoxins in infant cereals in the U.S. market by LC-MS MS using a stable isotope dilution assayFood Control72(Part A)27-35(2017)

Padanamide A is a bacterial metabolite originally isolated from a marine Streptomyces species. It is active against five strains of P. falciparum (EC50s = 160-340 nM), is not cytotoxic to HEK293 or HepG2 human cell lines, but is cytotoxic to Jurkat T lymphocytes with an IC50 value of approximately 60 μg/ml.

Darinaparsin is a dimethylated arsenic linked to glutathione. It is cytotoxic to DU145, LNCaP, and PC3 prostate cancer cells (IC50s = 5-10 µM) and patient-derived primary prostate cancer cells (IC50s = 2.5-20 µM), as well as Jurkat T cell lymphoma and L540 Hodgkin lymphoma cells (IC50s = 2.7 and 1.3 µM, respectively). [1][2] It decreases the tumor-initiating subpopulation in DU145 and PC3 cells and halts the cell cycle in the G2 M phase. Darinaparsin decreases transcription of Gli-2, a transcription factor that mediates Sonic hedgehog signaling, when used at a concentration of 1.5 but not 3 µM. It decreases SHP1 phosphatase activity and increases ERK phosphorylation. [2] Darinaparsin reduces tumor growth in DU145 and PC3 prostate cancer mouse xenograft models when administered at a dose of 100 mg kg every other day.[1]

CAY10774 is an inhibitor of the protein-protein interaction between programmed cell death 1 (PD-1) and its ligand PD-L1 (IC50= 15 nM in a homologous time-resolved fret (HTRF) assay).1It increases the activation of Jurkat cells expressing PD-1 in co-culture with artificial antigen-presenting cells (aAPCs) expressing PD-L1 (EC50= 6.6 μM in a reporter assay). CAY10774 increases surface expression of PD-1 on primary human CD4+and CD8+T cells co-cultured with aAPCs. 1.Konieczny, M., Musielak, B., Kocik, J., et al.Di-bromo-based small-molecule inhibitors of the PD-1/PD-L1 immune checkpointJ. Med. Chem.63(19)11271-11285(2020)

Malformin C is a natural fungus-derived bicyclic pentapeptide that has antibacterial properties, particularly against species of Bacillus. Malformin C potently blocks the ability of bleomycin to induce G2 arrest in human T-cell leukemia-derived Jurkat cells (IC50 = 0.9 nM). It less potently abrogates colchicine-induced M phase arrest in Jurkat cells (IC50 = 24 nM). Malformin C inhibits cell growth dose-dependently in Colon 38 and HCT 115 cancer cells (IC50s = 0.27 and 0.18 μM, respectively) but has a low therapeutic index against cancer xenografts when tested in mice.

4-Maleimidosalicylic acid is a polar maleimide compound that does not exhibit suppressive effects on IL-2 production in JURKAT T cells.

Nelarabine (GW 506U78) 是一种嘌呤核苷酸类似物，为DNA 合成抑制剂，对肿瘤细胞的IC50为0.067-2.15 μM，可作用于T 细胞急性淋巴细胞白血病。

BMS-554417 is a novel inhibitor of IGF-IR, which inhibits IGF-IR and insulin receptor kinase activity and proliferation in vitro, and reduces tumor xenograft size in vivo. In a series of carcinoma cell lines, the IC50 for proliferation ranged from 120 nmol L (Colo205) to >8.5 micromol L (OV202). BMS-554417 treatment inhibited IGF-IR and insulin receptor signaling through extracellular signal-related kinase as well as the phosphoinositide 3-kinase Akt pathway, as evidenced by decreased Akt phosphorylation at Ser473. At doses that inhibited proliferation, the compound also caused a G0-G1 arrest and prevented nuclear accumulation of cyclin D1 in response to LR3 IGF-I. In Jurkat T-cell leukemia cells, this agent triggered apoptotic cell death via the mitochondrial pathway. BMS-554417 was orally bioavailable and significantly inhibited the growth of IGF1R-Sal tumor xenografts in vivo. BMS-554417 is a member of a novel class of IGF-IR insulin receptor inhibitors that have potential......