TAT-CN21 

TAT-CN21 is a potent CaMKII inhibitor with an IC₅₀ of 77.2 nM. TAT-CN21 inhibits both calcium/calmodulin-dependent and autonomously activated CaMKII, blocks glutamate-induced translocation of CaMK IIα, and reverses the enhanced phosphorylation of CaMKII at Thr286 following excitotoxic injury. TAT-CN21 shows application potential in studies related to ischemic stroke by reducing neuronal excitotoxicity and exacerbating pre-existing long-term neuronal death prior to injury. TAT-CN21 improves definitive behaviors in rats with residual nerve injury without altering indicators such as mechanical/thermal hyperalgesia or spatial memory. TAT-CN21 can also be used in studies related to neuropathic pain^[1][2].

Tat-CN21 (0.1-50 μM; 24 h) dose-dependently protects 7-8 DIV primary rat cortical neurons against glutamate/glycine-induced excitotoxic injury when administered 20 minutes prior to injury, with the optimal efficacy observed at 2-10 μM^[1].
Tat-CN21 (10 μM; 1 h-2 h) protects primary rat cortical neurons at 7-8 DIV against glutamate/glycine-induced excitotoxic injury^[1].
Tat-CN21 (10 μM; 8-24 h) exacerbates submaximal dose glutamate/glycine-induced excitotoxicity in 7-8 DIV primary rat cortical neurons, and post-injury overnight treatment with Tat-CN21 also increases neuronal death^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

TAT-CN21 (5 μM; bilateral stereotaxic microinjection into rACC; once daily; 7 consecutive days) partially reverses pain-related aversion by reducing Ca²⁺/calmodulin-dependent protein kinase II-Thr286 phosphorylation in neuropathic pain rats, without altering hyperalgesia or spatial memory^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

3989.65

C₁₆₉H₃₀₃N₆₉O₄₃

Solid

White to off-white

Tyr-Gly-Arg-Lys-Lys-Arg-Arg-Gln-Arg-Arg-Arg-Lys-Arg-Pro-Pro-Lys-Leu-Gly-Gln-Ile-Gly-Arg-Ser-Lys-Arg-Val-Val-Ile-Glu-Asp-Asp-Arg

YGRKKRRQRRRKRPPKLGQIGRSKRVVIEDDR

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Ashpole NM, et al. Excitotoxic neuroprotection and vulnerability with CaMKII inhibition. Mol Cell Neurosci. 2011;46(4):720-730.  [Content Brief]

  [2]. Gao X, et al. Activation of the N-methyl-D-aspartate receptor and calcium/calmodulin-dependent protein kinase IIα signal in the rostral anterior cingulate cortex is involved in pain-related aversion in rats with peripheral nerve injury. Behav Brain Res. 2023;452:114560.  [Content Brief]