cysteine residue

N-Ethylmaleimide (NEM) is a reagent for alkylation of free sulfhydryl groups, a cysteine protease inhibitor used in experimental biochemistry. N-Ethylmaleimide is also a deubiquitinating enzyme inhibitor that specifically inhibits phosphate transport in mitochondria.

MS8511, a selective covalent irreversible inhibitor of G9a GLP, targets a cysteine residue at the substrate binding site, displaying IC50 values of 100 nM (G9a) and 140 nM (GLP), alongside Kd values of 44 nM (G9a) and 46 nM (GLP). This compound effectively reduces cellular H3K9me2 levels and boosts antiproliferation activity, making it applicable in cancer research involving brain, breast, ovarian, lung, bladder, melanoma, and colorectal cancers, as well as studies on Alzheimer's disease (AD), sickle cell disease, and Prader−Willi syndrome (PWS) [1].

THZ1 (CDK7 inhibitor) is a selective covalent inhibitor of CDK7, exhibiting binding affinity to the cysteine residue located at the outer end of the classical kinase domain, thus conferring high selectivity for CDK7, with an IC50 of 3.2 nM.

Peptide M is a synthetic Peptide, 50 aa, derived from streptococcus M protein, containing an additional c-terminal cysteine residue.

Melittin (C-Term Cysteine labeled) TFA is a cell-toxic peptide from bee venom. The peptide has a cysteine residue at the C-terminus and can be used for the synthesis of membrane-lysing polymers.

CL2A-SN-38 is a drug-linker conjugate composed of a potent a DNA Topoisomerase I inhibitor SN-38 and a linker CL2A to make antibody drug conjugate (ADC).. CL2A-SN-38 is composed of a potent a DNA Topoisomerase I inhibitor SN-38 and a linker CL2A to make antibody drug conjugate (ADC). CL2A-SN-38 provides significant and specific antitumor effects against a range of human solid tumor types. CL2A is a noncleavable complicated PEG8- and triazole-containing PABC-peptide-mc linker. CL2A is cleavable through pH sensitivity, giving rise to bystander effect, and binds the antibody at a cysteine residue via a disulfide bond. .

2'-Thioadenosine (PD157432) serves as a selective and irreversible inhibitor of ErbB-1 and ErbB-2 tyrosine kinases, demonstrating an IC50 value of 45 µM against ErbB-2. It achieves covalent inactivation of ErbB-1 through modification of a cysteine residue within the enzyme's active site [1].

MS8511 (hydrochloride) is a specific covalent and irreversible inhibitor of G9a GLP, targeting the cysteine residue at the substrate binding site. It has an IC50 of 100 nM for G9a and 140 nM for GLP, with Kd values of 44 nM for G9a and 46 nM for GLP. This compound reduces intracellular H3K9me2 levels and enhances antiproliferative activity, making it useful for studying various cancers, including brain, breast, ovarian, lung, bladder cancers, melanoma, and colorectal cancer, as well as other diseases like Alzheimer's disease (AD), sickle cell disease, and Prader-Willi syndrome (PWS).

Poseltinib is an orally active, selective, and irreversible Bruton's tyrosine kinase (BTK) inhibitor, exhibiting a half-maximal inhibitory concentration (IC 50) of 1.95 nM. It demonstrates 0.3, 2.3, and 2.4-fold greater selectivity for BTK over BMX, TEC, and TXK, respectively. This compound covalently binds to BTK's active site at the cysteine 481 residue, effectively inhibiting signaling pathways mediated by the B cell receptor (BCR), Fc receptor (FcR), and Toll-like receptor (TLR).

FLAG-Cys is a Flag peptide modified with an additional cysteine (Cys) residue, recognized for its immunogenicity [1].

AM841, a high-affinity electrophilic ligand, covalently interacts with a cysteine residue in helix six, thus activating the CB1 cannabinoid receptor. It diminishes forskolin-stimulated cAMP accumulation and slows gastrointestinal motility [1] [2].

Human α-Defensin 6, a 32-residue, cysteine-rich peptide, plays a crucial role in mucosal immunity by inhibiting bacterial invasion through the formation of ordered self-assembly fibrils and nanonets, which bind to bacterial surface proteins and entangle the bacteria. Additionally, Human α-Defensin 6 impedes biofilm formation by C. albicans [1] [2].

Leptomycin B (GMP) refers to the GMP grade reagents of Leptomycin B. Leptomycin B (LMB) is a potent inhibitor of the nuclear export of proteins and is a potent antifungal antibiotic blocking the eukaryotic cell cycle. Leptomycin B inactivates CRM1 exportin 1 by covalent modification at a cysteine residue.

CL2A is a pH-sensitive, cleavable PEG8- and triazole-containing PABC-peptide-mc linker, characterized by its ability to induce a bystander effect. It forms a disulfide bond with an antibody at a cysteine residue. Labetuzumab govitecan utilizes this linker for its drug conjugation[1].

Epsilon-V1-2, a Cys-conjugated, is a biologically active peptide known as the εPKC-specific inhibitor. It hampers εPKC functionality by obstructing its translocation and the phosphorylation of MARCKS, additionally perturbing εPKC's interaction with its anchoring protein, εRACK. The peptide includes a cysteine residue at its C-terminus, facilitating the formation of potential disulfide bonds with carrier proteins. Pyroglutamyl formation can occur spontaneously at the N-terminus if glutamine or glutamic acid is present, enhancing peptide stability against gastrointestinal proteases. Pyroglutamyl peptides, a recognized subset, are accounted for in the peptide's purity during HPLC analysis.

HC-258 is a direct TEAD inhibitor that forms a covalent bond with Cys380, a cysteine residue of TEAD proteins, and reduces the transcriptional levels and inhibits the migration of CTGF, CYR61, AXL and NF2 in MDA-MB-231 cells.

Illudalic acid, a potent and selective Leukocyte antigen-related (LAR) phosphatase inhibitor, has an IC 50 value of 1.30 µM. It inhibits LAR phosphatase by covalently binding to the catalytic cysteine residue [1] [2].

Olmutinib is a novel third-generation epidermal growth factor receptor (EGFR) mutation-specific tyrosine kinase inhibitor, used in the treatment of T790M mutation positive non-small cell lung cancer. Olmutinib covalently binds a cysteine residue near the kinase domain of mutant EGFRs to prevent phosphorylation of the receptor. EGFRs are frequently over-expressed in lung cancer and contribute to activation of the phosphoinositide 3-kinase and mitogen-activated protein kinase pathways which both promote cell survival and proliferation. By inhibiting EGFR activation, Olmutinib attenuates the activation of these tumor-promoting pathways. In the first phase I II clinical study of Osimertinib, 800 mg day was chosen as the dose for subsequent studies, and the dose-limiting toxicity and maximum tolerated dose was not reached. Olmutinib received breakthrough therapy designation in the United States in December 2015 and was approved for use in Korea in May 2016.

Cys(Npys)-TAT (47-57), a peptide fragment corresponding to the transduction domain of the TAT peptide, contains an activated cysteine residue C and can electrostatically interact with plasmid DNA. Notably, TAT is a small nuclear transcriptional activator protein encoded by HIV-1 [1].

cTEV6-2 covalently inhibits the Tobacco Etch Virus protease (TEV protease) by binding to its cysteine residue (C151), with an IC50 of 81.7 nM.

Leptomycin B (LMB) is a potent inhibitor of the nuclear export of proteins and is a potent antifungal antibiotic blocking the eukaryotic cell cycle. Leptomycin B inactivates CRM1 exportin 1 by covalent modification at a cysteine residue.