Kn 93

Manufactured by Bio-Techne

Sourced in United Kingdom, United States

KN-93 is a chemical compound that acts as a specific inhibitor of calcium/calmodulin-dependent protein kinase II (CaMKII). It functions by blocking the activity of CaMKII, a key enzyme involved in various cellular processes.

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Lab products found in correlation

Bicuculline, by Bio-Techne (4 mentions) Sto 609, by Bio-Techne (4 mentions) Mk 801, by Bio-Techne (3 mentions) Sp600125, by Bio-Techne (3 mentions) U0126, by Bio-Techne (3 mentions) Kn 62, by Bio-Techne (3 mentions) Bapta am, by Thermo Fisher Scientific (2 mentions) Nimodipine, by Abcam (2 mentions) Kt5720, by Bio-Techne (2 mentions) Rp camp, by Merck Group (2 mentions) Kribb11, by Bio-Techne (2 mentions) U0126, by Cell Signaling Technology (2 mentions) Cyclosporin a, by Bio-Techne (2 mentions) Pd98059, by Bio-Techne (2 mentions) Ly294002, by Bio-Techne (2 mentions) U73122, by Bio-Techne (2 mentions) Gf109203x, by Bio-Techne (2 mentions) Dnase 1, by Thermo Fisher Scientific (2 mentions) Dimethyl sulfoxide (dmso), by Merck Group (2 mentions) Pierce bca protein assay kit, by Thermo Fisher Scientific (2 mentions)

Close spelling variants of this product

KN-93 phosphate (2 citations)

35 protocols using kn 93

Surgical Placement of Cannulae in Rat Nucleus Accumbens

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Surgical procedures in rats were performed at the age of 7 weeks. Bilateral guide cannulae (Plastics One, 23G, Bilaney, Düsseldorf, Germany) were placed in the NAc core region (anteroposterior: ±1.6 mm, mediolateral: ±2.3 mm, dorsoventral: −7.2 mm; measurements given relative to bregma) or in the NAc shell region (anteroposterior: ±1.6 mm, mediolateral: ±2 mm, dorsoventral: −8.4 mm; measurements given relative to bregma). Guide cannulae were fixed to the animals’ skulls by two stainless steel screws and dental cement. Dummy cannulae were used to prevent blockage. Post operation, animals were provided with analgesia as well as a 5-day recovery period prior to behavioral testing.
KN-93 was prepared to a concentration of 12 µg/µL (dissolved in distilled water). On CPP test day, rats received a single infusion of KN-93 (6 µg/0.5 µL/side) [1 (link)] (Tocris Bioscience, Bristol, UK), a specific CaMKII inhibitor, or vehicle (distilled water). Infusions were performed for approximately 2 min and then the infusion cannulae were left in place for 3 min to prevent back-flow. Animals were kept in their home cages for 30 min before CPP testing was performed.
Correct cannula placement for animals that received infusions was ensured after the end of the behavioral experiments (Figure A2A).

Amaral I.M., Scheffauer L., Langeder A.B., Hofer A, & El Rawas R. (2021). Rewarding Social Interaction in Rats Increases CaMKII in the Nucleus Accumbens. Biomedicines, 9(12), 1886.

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Pharmacological Modulation of Neuronal Activity

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Drugs (Sigma, µM) were AP5 (100), AMPA (10), bicuculline (10), CsCl (2 mM), KA (20), ketanserin (1), KN-93 (1), MK-801 (50), NiCl₂ (50), nifedipine (50–75), NMDA (30 or 50), tatCN21 and tatCtrl (15, synthesized by K.U.B.), and TBOA (100, Tocris). Drugs were dissolved in ACSF (0.001% DMSO as needed) and tatCN21 and tatCtrl were dissolved in water before into the internal electrode solution.

Turecek J., Yuen G.S., Han V.Z., Zeng X.H., Bayer K.U, & Welsh J.P. (2014). NMDA RECEPTOR ACTIVATION STRENGTHENS WEAK ELECTRICAL COUPLING IN MAMMALIAN BRAIN. Neuron, 81(6), 1375-1388.

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Inducing CREB Phosphorylation in Cortical Neurons

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To induce CREB phosphorylation, we stimulated cortical neurons with the indicated high [K⁺] solution at 37 °C for 10–300 s, and fixed the cells immediately after the stimulation (in 4% paraformaldehyde in PBS, with 20 mM EGTA and 4% (w/v) sucrose), or incubated the cells in culture media for 90 min at 37 °C before fixation. Where indicated, drugs were added 30 min before and included throughout the stimulation. All K⁺-rich stimulation solutions contained 0.5 μM TTX (Ascent Scientific) to block action potentials. In addition, when stimulating cortical neurons, 10 μM NBQX (Ascent Scientific) and 10 μM APV (Ascent Scientific) were included to block AMPA and NMDA receptors, respectively. 4 mM K Tyrode’s consisted of (in mM): 150 NaCl, 4 KCl, 2 MgCl2, 2 CaCl2, 10 HEPES, 10 glucose, pH 7.4. When stimulating with elevated [K⁺], Na⁺ was adjusted to maintain osmolarity. To block: CaM Kinases, KN93 (Tocris) was used at 4uM; to block Ca_V1 channels, Nimodipine (abcam) was used at 10uM; to block CaMKK, STO609 (Tocris) was used at 3.3uM; to block PP2A, okadaic acid (Tocris) was used at 20 nM; to block PP1 and PP2A, okadaic acid (Tocris) was used at 2uM.
Cells were loaded with Ca²⁺ chelators EGTA-AM and BAPTA-AM (Life Technologies), used at 200uM, along with 1:1000 Pluronic F-127 (Life Technologies) 45 min before stimulation.

Cohen S.M., Li B., Tsien R.W, & Ma H. (2015). Evolutionary and functional perspectives on signaling from neuronal surface to nucleus. Biochemical and biophysical research communications, 460(1), 88-99.

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Peptide Synthesis and Characterization

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l-Glutamine, fetal bovine serum, penicillin, streptomycin, amphotericin B, Hanks’ salts, trypsin, DMEM, and (4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) were from PanEco, Moscow, Russia. 2′,7′-Dichlorodihydrofluorescein diacetate (DCFH-DA), HEPES, DMSO, d-glucose, MPP⁺, KCN, MPP⁺, l-NAME, tert-butyl hydroperoxide, and bovine serum albumin were from Sigma-Aldrich, St. Louis, MO, USA. 666-11, SB 202190, SP 600125, salirasib, FIPI, KN-93, ML-193, PSB C5, HA-1004, U-0126, KT-5720, and U-73 were from Tocris Bioscience, Bristol, UK. Total RNA Purification kit was from Jena Biosciences, Jena, Germany. MMLV reverse transcription kit and qPCR master mix qPCRmix-HS SYBR were from Evrogen, Moscow, Russia. cAMP determination kit and BrdU cell proliferation assay kit were from Abcam, Cambridge, MA, USA. DNase I was from Thermo Fisher Scientific, Waltham, MA, USA.
The peptide was synthesized by methods of classical peptide chemistry in solution using both protected and free L-amino acids, as described earlier [49 (link)]. Purity of the final compound was not less 98% (HPLC analysis, Supplementary S2).

Akimov M.G., Fomina-Ageeva E.V., Dudina P.V., Andreeva L.A., Myasoyedov N.F, & Bezuglov V.V. (2021). ACTH(6–9)PGP Peptide Protects SH-SY5Y Cells from H2O2, tert-Butyl Hydroperoxide, and Cyanide Cytotoxicity via Stimulation of Proliferation and Induction of Prosurvival-Related Genes. Molecules, 26(7), 1878.

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TGF-β1-Induced Epithelial Transformation

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HK-2 cells (American Type Culture Collection, VA, USA) were grown in keratinocyte-serum free medium (Thermofisher, MA, USA) with 10% fetal bovine serum in a 5% CO₂ humidified incubator at 37 °C. The cells were then treated with recombinant human TGF-β1 (2 ng/mL, R&D System, MN, USA) for 48 h with a combination of NMDA (50 μM, Tocris, MN, USA), MK-801 (10 μM, Tocris), or KN-93 (10 μM, Tocris).

Zhou J., Liu S., Guo L., Wang R., Chen J, & Shen J. (2020). NMDA receptor-mediated CaMKII/ERK activation contributes to renal fibrosis. BMC Nephrology, 21, 392.

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Cadmium-Induced Osteoblast Cytotoxicity

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Cells were plated at different densities depending on the assay. After 24 h, treatment was initiated with 0.1–10 μM CdCl₂ (Sigma–Aldrich, St. Louis, MO), 5 μM calmodulin-dependent PDE inhibitor CGS-9343β (Santa Cruz Biotechnology, CA, USA), 5 μM or 10 μM CAMKK inhibitor STO-609 (Tocris, Bristol, UK), 2.5 μM CAMKII inhibitor KN-93 (Tocris, Bristol, UK), or a co-treatment of CdCl₂ and inhibitor for 24 or 48 h (ATCC, Manassas, VA). For the cytotoxicity studies controls received OPTI-MEM serum-free medium only and for inhibitor studies the controls received OPTI-MEM serum-free medium containing 0.01% or less DMSO. A cytotoxicity profile using the MTT assay determined that 5 μM CGS-9343β, 5 μM or 10 μM STO-609, and 2.5 μM KN-93 were not cytotoxic and these concentrations were used for co-treatment experiments (data not shown). The CdCl₂ concentrations used are within the concentration range and exposure time reported in the literature (Pulido and Parrish, 2003 (link); Liu and Templeton, 2007 (link); Chen et al., 2011 ) and specifically for osteoblast cultures (Martineau et al., 2010 (link); Arbon et al., 2012 (link); Liu et al., 2014 (link), 2016 ).

Ha T.T., Burwell S.T., Goodwin M.L., Noeker J.A, & Heggland S.J. (2016). Pleiotropic roles of Ca+2/calmodulin-dependent pathways in regulating cadmium-induced toxicity in human osteoblast-like cell lines. Toxicology letters, 260, 18-27.

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Pharmacological Modulation of D4R in Synaptic Transmission

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The D4R antagonist L-745, 870 (Sigma) was first dissolved in dimethyl sulfoxide (DMSO) to make a stock solution and stored at 4 °C. This stock solution was then diluted in ACSF to a final concentration of 50 nM, ensuring that the final DMSO concentration did not exceed 0.1%. These concentrations were used as they did not affect basal synaptic transmission^{33 (link)}. The D4R agonists, PD 168077 (Sigma) and Ro-10-5824 (Tocris), were both used at 0.1 µM and anisomycin (Sigma), a protein synthesis inhibitor, and KN93 (Sigma), a CaMKII inhibitor were used at a concentration of 25 µM and 1 µM respectively. PD 168077 (Sigma), Ro-10-5824 (Tocris), anisomycin and KN93 were dissolved in DMSO to make stock solutions and later were dissolved in ACSF. The NMDA antagonist, AP5 (Sigma) was dissolved in water and was used at 50 µM concentration.

Navakkode S., Chew K.C., Tay S.J., Lin Q., Behnisch T, & Soong T.W. (2017). Bidirectional modulation of hippocampal synaptic plasticity by Dopaminergic D4-receptors in the CA1 area of hippocampus. Scientific Reports, 7, 15571.

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Osteoclast Differentiation Assay

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C3H10T1/2‐EV (empty virus) or C3H10T1/2‐Wnt1 cells were seeded in 96‐well plates at the density of 1.68 × 10⁴ cells/well. After attachment to the bottom of the wells, C3H10T1/2 cells were treated with 10 μg/mL mitomycin C (Sigma‐Aldrich) for 2 hours followed by careful washing with PBS. Then Raw264.7 cells were plated on top of C3H10T1/2 cells at a density of 3 × 10³ cells/well. The cells were stimulated with 50 ng/mL RANKL to induce osteoclast differentiation. For the experiments with inhibitors, the co‐culture cells were continuously treated with 10 μM XAV939 (Tocris Bioscience, Bristol, UK), 10μM KN93 (Tocris), or 5 μM SP600125 (Tocris). The culture medium was changed every 2 days and TRAP staining was performed at indicated time points.

Wang F., Tarkkonen K., Nieminen‐Pihala V., Nagano K., Majidi R.A., Puolakkainen T., Rummukainen P., Lehto J., Roivainen A., Zhang F., Mäkitie O., Baron R, & Kiviranta R. (2019). Mesenchymal Cell‐Derived Juxtacrine Wnt1 Signaling Regulates Osteoblast Activity and Osteoclast Differentiation. Journal of Bone and Mineral Research, 34(6), 1129-1142.

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Glutamate and KN93 Receptor Binding

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The following chemicals were used for this study: glutamate (50 μM, Sigma-Aldrich) and KN93 (10 μM, Tocris Bioscience). [³H]CGP 54626 (30 Ci/mmol) was purchased from ANAWA Trading SA and CGP 56999A was kindly provided by Novartis.

Zemoura K., Balakrishnan K., Grampp T, & Benke D. (2018). Ca2+/Calmodulin-Dependent Protein Kinase II (CaMKII) β-Dependent Phosphorylation of GABAB1 Triggers Lysosomal Degradation of GABAB Receptors via Mind Bomb-2 (MIB2)-Mediated Lys-63-Linked Ubiquitination. Molecular Neurobiology, 56(2), 1293-1309.

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Pharmacological Inhibitors of Signaling Pathways

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OS47720 (abbreviated as OS47720), was initially provided by NexGenenix Pharmaceutical, Inc., NY with an original name of NXD30020, later by OncoSynergy, San Francisco, CA. KRIBB11, KN92 and KN93 was purchased from Tocris; RpcAMP and H89 was purchased from Sigma; LY294002 was purchased from LC labs; U0126 was purchased from Cell signal.

Wang B., Liu Y., Huang L., Chen J., Li J.J., Wang R., Kim E., Justicia C., Sakata K., Chen H., Planas A., Ostrom R.S., Li W., Yang G., McDonald M.P., Chen R., Heck D, & Liao F.F. (2016). A CNS-permeable Hsp90 inhibitor rescues synaptic dysfunction and memory loss in APP-overexpressing Alzheimer’s mouse model via an HSF1-mediated mechanism. Molecular psychiatry, 22(7), 990-1001.

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