jurkat

Necrostatin-1 (Nec-1) is a necrotic apoptosis inhibitor and RIP1 inhibitor with specificity. Necrostatin-1 inhibits TNF-α-induced necrotic apoptosis. Necrostatin-1 also inhibits IDO.

2-Nitrobenzoic acid (o-Nitrobenzoic acid) is a antiproliferation agent. 2-Nitrobenzoic acid shows IC50 of 8.3 μM to jurkat cell line expressing T type calcium channel alpha 1H or its splice variant delta 25.

CTA 056 is an interleukin-2 induced T cell kinase (ITK) inhibitor, inhibits the growth of MOLT-4 xenograft tumors in mice, induces apoptosis in Jurkat cells, and can be used in the study of autoimmune disorders and T cell malignancies.

Neoandrographolide (Neoandrographiside) has potent hypolipidemic effect and protects the cardiovascular without significant liver damage.Neoandrographolide has anti-inflammatory effect, might result from inhibition of iNOS and COX-2 expression through inhibiting p38 MAPKs activation.Neoandrographolide as chemosensitizer in S-Jurkat and X chromosome-linked inhibitor of apoptosis protein (XIAP)-overexpressing Jurkat cells, a model for chemoresistance.

LH1306 is an inhibitor of the interaction between programmed cell death 1 (PD-1) and its ligand PD-L1 that has an IC50 value of 25 nM in a homologous time-resolved fluorescence (HTRF) assay.1 It increases the activation of Jurkat cells expressing PD-1 in co-culture with U2OS or CHO cells expressing PD-L1 (EC50s = 334 and 4,214 nM, respectively, in reporter assays). |1. Basu, S., Yang, J., Xu, B., et al. Design, synthesis, evaluation, and structural studies of C2-symmetric small molecule inhibitors of programmed cell death-1/programmed death-ligand 1 protein-protein interaction. J. Med. Chem. 62(15), 7250-7263 (2019).

TJ191 is a selective anti-cancer agent, targeting low TβRIII-expressing malignant T-cell leukemia/lymphoma cells.

LH1307 is an inhibitor of the interaction between programmed cell death 1 (PD-1) and its ligand PD-L1 that has an IC50 value of 3 nM in a homologous time-resolved fluorescence (HTRF) assay.1 It increases the activation of Jurkat cells expressing PD-1 in co-culture with U2OS or CHO cells expressing PD-L1 (EC50s = 79 and 763 nM, respectively, in reporter assays). |1. Basu, S., Yang, J., Xu, B., et al. Design, synthesis, evaluation, and structural studies of C2-symmetric small molecule inhibitors of programmed cell death-1/programmed death-ligand 1 protein-protein interaction. J. Med. Chem. 62(15), 7250-7263 (2019).

Chlorido[N,N'-disalicylidene-1,2-phenylenediamine]iron(III) is an inducer of ferroptosis.1 It induces ferroptosis, but not apoptosis or necroptosis, in NB1 cancer cells when used at a concentration of 3 μM.1 Chlorido[N,N'-disalicylidene-1,2-phenylenediamine]iron(III) inhibits proliferation of BJAB, NALM-6, Jurkat, MelHO, and MCF-7 cancer cells (IC50s = 0.07, 2.5, 1.5, 3, and 5 μM, respectively), as well as NALM-6 cells resistant to daunorubicin and vincristine when used at concentrations ranging from 0.04 to 0.125 μM.2 |1. Sagasser, J., Ma, B., Baecker, D., et al. A new approach in cancer treatment: Discovery of chlorido[N,N'-disalicylidene-1,2-phenylenediamine]iron(III) complexes as ferroptosis inducers. J. Med. Chem. 62(17), 8053-8061 (2019).|2. Lee, S.-Y., Hille, A., Kitanovic, I., et al. [FeIII(salophene)Cl], a potent iron salophene complex overcomes multiple drug resistance in lymphoma and leukemia cells. Leuk. Res. 35(3), 387-393 (2011).

7-Isopentenyloxy-gamma-fagarine has highly cytotoxicity against the MCF-7and Jurkat cell line. It has been used as a precursor for the chemical asymmetric synthesis of the enantiopure alkaloids: evoxine, anhydroevoxine and evodine.

PRO-HD1, a PROTAC (proteolysis-targeting chimera) HDAC6 degrader, effectively degrades HDAC6 in A549 cells and inhibits Jurkat cell proliferation with an IC50 of 5.8 µM [1].

ent-11alpha-Hydroxyabieta-8(14),13(15)-dien-16,12alpha-olide shows significant cytotoxic activity against ANA-1 and Jurkat cells with IC50 values 7.12 x 10(-3) and 1.79 x 10(-2) microM.

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)

JAK-IN-27, also known as compound 1, is an orally active, potent inhibitor of the JAKS family kinases, displaying inhibitory concentrations (IC50s) of 3.0 nM for TYK2, 7.7 nM for JAK1, and 629.6 nM for JAK3. Moreover, JAK-IN-27 impedes IFN-α2B-induced phosphorylation of STAT3 in Jurkat cells with an IC50 of 23.7 nM [1].

EPI-X4, an endogenous peptide fragment of human serum albumin (amino acids 408-423), serves as an antagonist to the chemokine (C-X-C motif) receptor 4 (CXCR4). It effectively prevents calcium mobilization and receptor internalization triggered by chemokine (C-X-C motif) ligand 12 (CXCL12) in HEK293 cells with CXCR4 expression, at concentrations between 0.8 and 1,000 µM. Moreover, EPI-X4 hampers the CXCL12-driven migration of both Jurkat T cells and human CD34+ hematopoietic stem cells. In an acute allergic airway hypereosinophilia mouse model, EPI-X4 intrinsically decreases Cxcr4-dependent inflammatory cell infiltration in airways at a dose of 16 µmol/kg. Additionally, increased urinary EPI-X4 levels, inversely related to glomerular filtration rate (GFR), are observed in chronic kidney disease patients, indicating its potential biomarker role.

Phytosphingosine is a phospholipid with anticancer properties. In cancer cells, Phytosphingosine induces cell apoptosis through activation of caspase 8 and translocation of Bax.

Z-AEVD-FMK is an irreversible inhibitor of caspase-10 and related caspases.[1] At 10 µM, it can prevent the initiation of Fas signaling by caspase-10 in Jurkat T lymphoma cells, preventing Bid cleavage into its active form, caspase cascade activation, and apoptosis.[2]

Apostatin-1 (Apt-1) is a novel TRADD inhibitor. Apostatin-1 can bind to a pocket on the N-terminal TRAF2 binding domain of TRADD.

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.

Irreversible MALT1 inhibitor. Suppresses T cell activation-induced cleavage of Bcl-10 in a dose-dependent manor. Reduces Jurkat cell adhesion to fibronectin. Cell permeable.

Carotegrast methyl (AJM300), an orally-active small molecule, can antagonize the α4 integrin receptor. It is a specific and dual α4β1/α4β7 integrin antagonist.

ITK Degrader 1, a highly selective interleukin-2-inducible T-cell kinase (ITK; DC50=3.6 nM in vivo in mice) degrader, induces rapid and prolonged degradation of ITK and effectively suppresses IL-2 secretion (EC50=35.2 nM, Jurkat cells) stimulated by anti-CD3 antibody in vivo. Additionally, it demonstrates favorable plasma exposure levels [1].

N-Myristoyl-Lys-Arg-Thr-Leu-Arg is a protein kinase C (PKC) inhibitor, demonstrating an IC50 value of 75 μM. It effectively inhibits IL-2 receptor induction and IL-2 production in the human leukemic cell line Jurkat [1].

TMX-4100 is a potent degrader of phosphodiesterase 6D (PDE6D), exhibiting high degradation selectivity towards PDE6D with DC50 values below 200 nM in MOLT4, Jurkat, and MM.1S cells. This compound holds significant potential for research pertaining to multiple myeloma.

Heraclenin has anticoagulant, and anti-inflammatory activities, it also has mutagenicity in Chlamydomonas reinhardii. Heraclenin can induce apoptosis in Jurkat leukemia cells, it has a strong clastogenic effect . (+)-Heraclenin displays significant levels

Milategrast is a chemical compound that functions as a potent cell adhesion inhibitor and cell infiltration inhibitor. In vitro studies have demonstrated its ability to effectively inhibit the adhesion of Jurkat cells to human fibronectin, with an IC50 value of less than 5 μM.

Nelarabine (GW 506U78) is a purine nucleoside analog and DNA synthesis inhibitor with IC50 from 0.067-2.15 μM in tumor cells.

LP-261 is a novel tubulin targeting anticancer agent that binds at the colchicine site on tubulin, inducing G2/M arrest.

LP23, a non-arylmethylamine PD-1/PD-L1 inhibitor (IC 50: 16.7 nM), exhibits anti-tumor activity through the restoration of immune cell function in HepG2/Jurkat T cells and induction of HepG2 cell death. Additionally, LP23 demonstrates in vivo efficacy in the B16-F10 tumor model (TGI=88.6% at 30 mg/kg) [1].

JAK-IN-26 (compound 2) is an orally active inhibitor of the Janus kinase (JAK) enzyme with favorable pharmacokinetic properties, exhibiting potency in suppressing IFN-α2B-induced STAT3 phosphorylation in Jurkat cells with an IC50 value of 17.2 nM [1].

CHDI 00484077, a potent and selective class IIa histone deacetylase (HDAC) inhibitor, demonstrates significant efficacy with IC50 values ranging from 10-30 nM in vivo and specific activity at 0.01 nM and 0.04 nM in HEK293 and Jurkat cells, respectively. It exhibits a 150-fold selectivity for class IIa over class I/IIb HDACs in cellular environments, indicating a high degree of specificity. Additionally, CHDI 00484077 is orally bioavailable and capable of crossing the blood-brain barrier (CNS penetrant).

Isobonducellin exhibits potent cytotoxic activity in Jurkat and HepG2 cells, while moderate growth inhibition against Colon205 cells.

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)

TMX-4116, a casein kinase 1α (CK1α) degrader, preferentially degrades CK1α in MOLT4, Jurkat, and MM.1S cells, exhibiting degradation concentration 50s (DC50s) below 200 nM. TMX-4116 is utilized in the research of multiple myeloma [1].

BMS-1001 hydrochloride is an orally active inhibitor of human PD-1/PD-L1 immune checkpoint with low-toxicity in cells.BMS-1001 alleviates the inhibitory effect of the soluble PD-L1 on the T-cell receptor-mediated activation of T-lymphocytes. BMS-1001 is capable of alleviating the PD-1/PD-L1 immune checkpoint-mediated exhaustion of Jurkat T-lymphocytes.

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

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]

Andrograpanin (19-HYDROXY-8(17),13-LABDADIEN-16,15-OLIDE) is a bioactive compound from Andrographis paniculata. Andrograpanin has anti-inflammatory and anti-infectious properties.

Boromycin is a boron-containing macrolide antibiotic that has been found in Streptomyces. Boromycin inhibits growth of B. subtilis (MIC = 0.05 μg/ml) and induces efflux of potassium ions from B. subtilis without affecting Na+/K+-ATPase activity. It decreases the synthesis of protein, RNA, and DNA in B. subtilis when used at a concentration of 0.05 μg/ml. It inhibits the growth of B. halodurans (MIC = 10 ng/ml) and inhibits the futalosine pathway of menaquinone synthesis in B. halodurans. Boromycin (3.4 nM) reverses bleomycin-induced cell cycle arrest at the G2 phase in Jurkat cells. It inhibits replication of the HIV-1 strains LAV-1 and RF and the HIV-2 strain LAV-2 in MT-4 cells (IC50s = 0.008, 0.11, and 0.007 μM, respectively). It also inhibits replication of a clinical isolate of HIV-1, strain KK-1, in MT-4 cells and peripheral blood mononuclear cells (PBMCs; IC50s = 0.14 and <0.1 μM, respectively).

TFRGAP-amide, human PAR-3-derived tethered ligand sequence which does not activate PAR-3 but rather activates PAR-1 and PAR-2, either in Jurkat or in other PAR-expressing cells.

2,5-Deoxyfructosazine is a pyrazine derivative that can be found in cured tobacco and is used as a flavoring agent in the food and tobacco industry. Pyrazines, including 2,5-deoxyfructosazine, can be produced either by pyrolytic decomposition of natural compounds or by the reaction of sugars with alcoholic ammonia. 2,5-Deoxyfructosazine is also formed by the breakdown of D-glucosamine at neutral pH. Like glucosamine, 2,5-deoxyfructosazine has DNA strand breakage activity and strongly inhibits IL-2 production by Jurkat cells stimulated with phytohemagglutinin (IC50 = ~1.25 mM).

Necrostatin 2 is an effective necroptosis inhibitor. Necrostatin 2 is also a RIPK1 inhibitor. EC50 for inhibition of necroptosis in FADD-deficient Jurkat T cells treated with TNF-α is 0.05 μM.

HPK1-IN-33 (compound 21), a Hematopoietic Progenitor Kinase 1 (HPK1) inhibitor, exhibits a high potency with a K_i of 1.7 nM. It effectively inhibits IL-2 production, demonstrating EC_50 values of 286 nM in Jurkat WT cells and >10000 nM in Jurkat HPK1 KO cells [1].

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)

S-Acetyl-L-glutathione is a derivative of glutathione .1 It increases intracellular GSH levels in primary fibroblasts derived from patients with glutathione synthetase deficiency when used at a concentration of 50 μM. S-Acetyl-L-glutathione (5 mM) induces apoptosis in Daudi, Raji, and Jurkat lymphoma cells.2 It inhibits the replication of herpes simplex virus 1 (HSV-1) in human foreskin fibroblasts when used at concentrations of 5 and 10 mM.3 S-Acetyl-L-glutathione (6.25 μg/g per day) increases survival in a mouse model of HSV-1 infection.

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......

Cuspidiol shows cytotoxicity against Jurkat T cell clone E6.1 at 7.3 ug/mL.

KTX-Sp2, a potassium channel toxin, effectively blocks exogenous voltage-gated potassium channels Kv1.1, Kv1.2, and Kv1.3, as well inhibits the endogenous Kv1.3 channel and suppresses Ca2+ signaling in Jurkat T cells. Additionally, KTX-Sp2 inhibits IL-2 secretion from activated Jurkat T cells [1].

HDAC4 CHDI Degrader 11 is a potent, selective degrader of HDAC4 (PROTAC) with DC_50 values of 4 nM and 6 nM in Jurkat E6-1 and Jurkat cells, respectively. This compound integrates the class IIa HDAC inhibitor trifluoromethyloxadiazole with a ligand for the Von Hippel-Lindau (VHL) protein through a linker. Demonstrating significant efficacy, HDAC4 CHDI Degrader 11 achieves a DC_50 value of 1 nM in a mouse cell model of Huntington's disease. For enhanced degradation in neuroblastoma cell lines, it can be administered alongside the P-glycoprotein inhibitor, Elacridar.

Necrostatin-5 (Nec-5) is a selective inhibitor of RIP1 kinase and a cell necrosis inhibitor that prevents the death of Fadd-deficient Jurkat cells treated with TNF-α with an EC50 value of 240 nM.

TDO-IN-1 is an orally active, potent, and selective inhibitor of tryptophan 2,3-dioxygenase (TDO), which inhibits indoleamine-2,3-dioxygenase.TDO-IN-1 has antitumor activity and is able to act by reversing local immune tolerance in tumor tissues.

HT-2 Toxin, a deacetylated metabolite of T-2 toxin, impairs protein synthesis and hinders cell proliferation in plants.