Pamapimod

Manufactured by Selleck Chemicals

Sourced in United States

Pamapimod is a laboratory equipment product. It is a specialized device used for biochemical and molecular biology research applications.

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Lab products found in correlation

Il 33, by Thermo Fisher Scientific (1 mentions) Gm csf, by Thermo Fisher Scientific (1 mentions) Il 18, by Thermo Fisher Scientific (1 mentions) Il 12, by Thermo Fisher Scientific (1 mentions) Tapi 1, by Merck Group (1 mentions) Moxifloxacin, by Cayman Chemical (1 mentions) Thalidomide, by Merck Group (1 mentions) Bromopyruvic acid, by Merck Group (1 mentions) Cyclosporin a, by Cayman Chemical (1 mentions) Bms 582949, by Selleck Chemicals (1 mentions) Necrostatin 1, by Cayman Chemical (1 mentions) Rifampicin, by AppliChem (1 mentions) Doramapimod, by Cayman Chemical (1 mentions) Z vad fmk, by Selleck Chemicals (1 mentions) Dexamethasone (dex), by Merck Group (1 mentions) Gentamicin, by Merck Group (1 mentions) Staurosporine, by Merck Group (1 mentions) Rapamycin, by Selleck Chemicals (1 mentions) Cetuximab, by Merck Group (1 mentions) Gw5074, by Selleck Chemicals (1 mentions)

3 protocols using pamapimod

Modulation of Inflammatory Signaling Pathways

Cited 1 time

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Recombinant human TNFα (Rhtnf-a, Invivogen/bioconnect,France), Recombinant Human Interferon-γ (11343536, Immunotools, Germany). Cetuximab (5 mg/ml; Merck serono, USA), rituximab (10 mg/ml; Roche, Switzerland), rapamycin (50 nM; Selleckchem, Germany), PD98059 (50 μM; Selleckchem), GW5074 (20 μM; Selleckchem), LY294002(25 μM; Selleckchem),SP600125 (20 μM; Selleckchem). Pamapimod (0,5uM Selleckchem), JSH-23(10uM, Selleckchem), and T-5224(20uM, Apexbt, USA). The concentration of GW5074, SP600125, LY-294,002, PD98059, rapamycin was chosen on basis of previous results [22 (link)]. The concentration of Pamapimod (0,5uM Selleckchem), JSH-23(10uM, Selleckchem), and T-5224(20uM, Apexbt) was according to instruction of the manufacturer.

Ma W., Concha-Benavente F., Santegoets S.J., Welters M.J., Ehsan I., Ferris R.L, & van der Burg S.H. (2018). EGFR signaling suppresses type 1 cytokine-induced T-cell attracting chemokine secretion in head and neck cancer. PLoS ONE, 13(9), e0203402.

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Optimizing Cytokine-Induced NK Cell Activation

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Enriched NK cells (unless mentioned otherwise, 5 × 10⁴ per well in triplicate per condition) were cultured overnight in the presence of 60 U/ml of IL-2. Various concentrations of IL-12, IL-18, or IL-33 or (Peprotech®, Rocky Hill, NJ) were added to cultures for 6–16 h. Cell-free supernatant was collected and analyzed by ELISA for levels of human IFN-γ, TNF, and GM-CSF (Invitrogen, Waltham, MA). For inhibition of MAPK activity, 125 nM (measured IC₅₀) of the selective p38 MAPK inhibitor Pamapimod (R-1503, Selleckchem, Houston, TX) was added 150 min prior to cytokine stimulation. The inhibition of MK2 (p38/mitogen-activated protein kinase-activated protein kinase 2) was performed with 5 μM MK2 IV (CAYMAN chemical, Ann Arbor, MI). The inhibition of ADAM-17 (a disintegrin and metalloprotease-17) was performed by adding 8 μM TAPI-1 (Merck Millipore, Burlington, MA). TAPI-1 and MK2 IV were added 60 min before cytokine stimulation. At the tested concentrations, none of the tested inhibitor affected cell viability (data not shown).

Ochayon D.E., Ali A., Alarcon P.C., Krishnamurthy D., Kottyan L.C., Borchers M.T, & Waggoner S.N. (2020). IL-33 promotes type 1 cytokine expression via p38 MAPK in human NK cells. Journal of leukocyte biology, 107(4), 663-671.

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Pharmacological Screening Library Compounds

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Rifampicin was purchased from AppliChem. Bromopyruvic acid, dexamethasone, gentamicin, staurosporine, and thalidomide were purchased from Sigma-Aldrich. Cyclosporin A, doramapimod, moxifloxacin, necrostatin-1, necrostatin-5, and tacrolimus (FK506) were obtained from Cayman Chemicals. BMS-582949, pamapimod, and Z-VAD-FMK were purchased from Selleckchem. Puromycin dihydrochloride was from Carl Roth (Germany). GR agonist BI653048 was provided by the opnMe platform (Boehringer Ingelheim). The Prestwick chemical library was used for high-throughput screening.

Gräb J., Suárez I., van Gumpel E., Winter S., Schreiber F., Esser A., Hölscher C., Fritsch M., Herb M., Schramm M., Wachsmuth L., Pallasch C., Pasparakis M., Kashkar H, & Rybniker J. (2019). Corticosteroids inhibit Mycobacterium tuberculosis-induced necrotic host cell death by abrogating mitochondrial membrane permeability transition. Nature Communications, 10, 688.

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