cl2a

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].

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. .

CL2A-SN-38 consists of a CL2A linker and an anticancer compound, SN-38, which delivers active molecules within tumor cells and in the tumor microenvironment, often in conjunction with antibodies to make biologically active antibody-coupled reactive molecules (ADCs).

(S,R,S)-AHPC-(C3- PEG) 2- C6- Cl is a small molecule HaloPROTAC that incorporates the (S,R,S)-AHPC based VHL ligand and 2-unit PEG linker. (S,R,S)-AHPC-(C3- PEG) 2- C6- Cl is capable of inducing the degradation of GFP-HaloTag7 in cell-based assays[1].

CL2 Linker is a cleavableADC linker. CL2-SN-38 and CL2A-SN-38 are equivalent in drug substitution (~6), cell binding (Kd ~1.2 nM), cytotoxicity (IC50 ~2.2 nM), and serum stability in vitro (t1/2 ~20 hours)[1][2].