bystander effect

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).

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 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].

AuristatinS is a potent anti-tumor agent that serves as an Auristatin payload. It effectively reduces the bystander effect and decreases off-target toxicity. In the Karpas/KarpasBVR cell model, AuristatinS exhibits excellent tolerability. It can be used as the cytotoxic component in antibody-drug conjugates (ADCs) for treating various types of cancer.

MC-AcLys-GDEVD-PABC-Exatecan is a component of an antibody-drug conjugate (drug-linker conjugate for ADC) composed of an ADC linker (MC-AcLys-GDEVD-PABC) attached to the DNA topoisomerase I inhibitor, Exatecan. It operates by enhancing the release of small molecule drugs into the tumor microenvironment through a significant bystander effect, triggered by caspase-3-induced extracellular cleavage of the linker.