Calmodulin-Dependent Protein Kinase II 290-309 acetate is an effective antagonist of Ca2+/calmodulin-dependent protein kinase II (IC50 = 52 nM).

Calmodulin Binding Peptide 1, a potent CaM-binding peptide with picomolar (pM) affinity, originates from smooth muscle myosin light-chain kinase (MLCK peptide). It effectively blocks inositol trisphosphate (IP3)-induced calcium (Ca2+) release [1].

Calmodulin-Dependent Protein Kinase II (290-309) acetate is a potent antagonist of CaMK, exhibiting an IC50 of 52 nM for the inhibition of Ca2+/calmodulin-dependent protein kinase II [1].

Calmodulin Dependent Protein Kinase Substrate is a synthetic peptide that serves as a substrate for protein kinases and requires calcium ions (Ca 2+) and calmodulin (CaM) for activation. It specifically interacts with calmodulin-dependent protein kinases (CaMK). This compound is utilized in studies involving protein kinase activity [1].

Myristoylated Calmodulin Kinase IINtide (Myr-CaMKIINtide) serves as a selective and noncompetitive inhibitor of CaMKII [1].

Calmodulin-Dependent Protein Kinase II (290-309) is a potent CaMK antagonist with an IC50 of 52 nM for inhibition of Ca2+/calmodulin-dependent protein kinase II.

Calmodulin-Dependent Protein Kinase II (281-309) is a synthetic peptide that can be phosphorylated at Thr286 by PKC and inhibits CaM kinase II (IC50 = 80 nM).

Calmodulin-Dependent Protein Kinase Substrate Analog, a synthetic peptide substrate, is activated by Ca2+ and calmodulin (CaM). It serves as a substrate for protein kinases, leveraging a dependency on Ca2+ and CaM for its function [1].

CALP3 acetate is a potent Ca2+ channel blocker that activates EF hand motifs of Ca2+-binding proteins. CALP3 acetate can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin (CaM), Ca2+ channels and pumps.

Camstatin acetate binds calmodulin and inhibits neuronal nitric oxide synthase. Camstatin acetate is a functionally active 25-residue fragment of the single calmodulin-binding IQ motif of PEP-19.

CALP2 acetate is an antagonist of calmodulin showing high affinity for binding to the CaM EF-hand/Ca2+-binding site with a Kd of 7.9 µM. CALP2 acetate potently inhibits of adhesion and degranulation. CALP2 acetate is also a strong activator of alveolar macrophages. CALP2 acetate inhibits CaM-dependent phosphodiesterase activity and increases intracellular Ca2+ concentrations.

Autocamtide 2 TFA is a highly selective peptide substrate of calcium/calmodulin-dependent protein kinase II (CaMKII). Autocamtide 2 TFA can be used in the CaMKII activity assay.

CALP1 acetate is a calmodulin (CaM) agonist (Kd of 88 µM) that binds to the CaM EF-hand/Ca2+-binding site. CALP1 blocks calcium influx and apoptosis (IC50 of 44.78 µM) by inhibiting the open of calcium channel. CALP1 blocks glutamate receptor channels and blocks a store-operated nonselective cation channel. CALP1 activates CaM-dependent phosphodiesterase activity.

Syntide-2 acetate is a synthetic peptide recognized as a substrate by Ca2+/calmodulin-dependent protein kinase II (CaMKII; Km = 12 μM).

SK-MLCK M13 is a biologically active peptide representing the calmodulin (CaM)-binding domain of CaM target proteins, where CaM is a ubiquitous Ca2+ binding protein.

Autocamtide 2, amide is a substrate (100 μM final concentration) for CaMK family assays.Autocamtide-2 Peptide is a highly selective peptide substrate for calcium/calmodulin-dependent protein kinase II (CaMKII), a member of the CAMK Ser/Thr protein kinase

Autocamtide-2 is a highly selective peptide substrate for calcium/calmodulin-dependent protein kinase II (CaMKII), which belongs to the CAMK Ser/Thr protein kinase family.

NFAT Inhibitor acetate (VIVIT peptide acetate) is a cell-permeable and selective NFAT peptide inhibitor of calmodulin phosphatase-mediated NFAT dephosphorylation.

Cell-permeable calmodulin (CaM) agonist that binds to the EF-hand/Ca2+-binding site. Activates phosphodiesterase in the absence of Ca2+ and inhibits Ca2+-mediated cytotoxicity and apoptosis (IC50 = 33 μM).

Syntide-2 is a synthetic peptide recognized as a substrate by Ca2+/calmodulin-dependent protein kinase II (CaMKII; Km = 12 µM).

Cell-permeable calmodulin (CaM) agonist that binds to the EF-hand/Ca2+-binding site; produces CaM-dependent activation of phosphodiesterase. Also binds to cytoplasmic sites on other Ca2+ channels, including NMDA and HIV-1 gp120-activated channels, inhibit

Camstatin TFA, a 25-residue fragment derived from the IQ motif of PEP-19, effectively binds to calmodulin and inhibits neuronal nitric oxide (NO) synthase, demonstrating its functional activity [1].

Autocamtide-2-related inhibitory peptide is a highly specific and potent inhibitor of CaMKII with an IC50 of 40 nM.

Autocamtide-3, a selective substrate for CaMKII (Ca2+/calmodulin-dependent kinase II) (CaMK), comprises a 13-amino-acid peptide featuring Thr287 [1].

Neurogranin (48-76), mouse, is a peptide comprising residues 48-76 of Neurogranin, a post-synaptically exclusive calmodulin-binding protein that mediates NMDAR-driven synaptic plasticity by regulating the calcium-calmodulin (Ca2+-CaM) pathway [1].

Cell-permeable calmodulin (CaM) antagonist that binds to the EF-hand/Ca2+-binding site. CALP2 has been demonstrated to inhibit CaM-dependant phosphodiesterase activity and increase intracellular Ca2+ concentrations by modulating Ca2+-channel activity. CAL

Selective inhibitor of Ca2+-calmodulin-dependent protein phosphatase (calcineurin) (IC50 ~ 10 μM). Does not inhibit PP1, PP2A or CaM kinase II (IC50 > 100 mM).

An analog of PEP-19 with enhanced binding to and antagonism of calmodulin.

Myristoylated AC3-I is a biologically active peptide and a myristoylated variant of the Autocamtide-3-Derived Inhibitory Peptide (AC3-I). It acts as a highly specific inhibitor of Calmodulin-Dependent Protein Kinase II (CaMKII) with enhanced resistance to proteolysis. This compound is a derivative of Autocamtide-3, where the Thr-9 phosphorylation site is replaced by Ala.

CALP2 TFA, a potent calmodulin (CaM) antagonist with a dissociation constant (Kd) of 7.9 µM, exhibits high affinity for the CaM EF-hand/Ca2+-binding site. This compound effectively inhibits CaM-dependent phosphodiesterase activity and elevates intracellular Ca2+ concentrations. Furthermore, it significantly hinders adhesion and degranulation, while also acting as a robust activator of alveolar macrophages [1] [2] [3] [4].

CALP3 TFA is a potent Ca2+ channel blocker that activates EF-hand motifs of Ca2+-binding proteins. It can functionally mimic increased [Ca2+]i by modulating the activity of Calmodulin, Ca2+ channels, and pumps.

CALP3 TFA, a Ca2+-like peptide and potent Ca2+ channel blocker, activates EF hand motifs in Ca2+-binding proteins. It can mimic increased [Ca2+]i, modulating the activity of Calmodulin (CaM), Ca2+ channels, and pumps. This compound shows promise in controlling apoptosis in conditions like AIDS or ischemic neuronal loss [1] [2].

Calcineurin Autoinhibitory Peptide TFA is a selective inhibitor of Ca2+/calmodulin-dependent protein phosphatase (calcineurin), exhibiting an inhibitory concentration (IC50) of approximately 10 μM. This compound has been shown to protect neurons from excitatory neuronal death [1] [2].

Syntide 2 (TFA), a substrate peptide for Ca2+- and calmodulin (CaM)-dependent protein kinase II (CaMKII), selectively inhibits the gibberellin (GA) response without affecting constitutive and abscisic acid-regulated events [1].

CALP1 TFA, a calmodulin (CaM) agonist with a dissociation constant (Kd) of 88 µM, selectively binds to the CaM EF-hand/Ca2+-binding site, inhibiting calcium channel opening. This action blocks calcium influx and apoptosis with an IC50 of 44.78 µM, modulates glutamate receptor channel activity, and impedes a store-operated nonselective cation channel. Additionally, CALP1 TFA enhances CaM-dependent phosphodiesterase activity, denoting its multifaceted role in modulating cellular calcium dynamics [1] [2] [3] [4].