CPP44

FITC-labelled CPP44 (10 μM; 6 h) selectively penetrates myeloid leukemia K562 cells and hepatoblastoma HepG2 cells, but fails to penetrate HeLa, Lovo, A549, MCF7, U2OS or NHDF cells^[1].
FITC-labelled CPP44 (10 μM) can selectively penetrate some human hepatocellular carcinoma cell lines and primary AML cells, but shows no uptake in Hep3B and Huh-7 hepatocellular carcinoma cells^[1].
FITC-labelled CPP44 (10 μM; 3 h) potently and selectively penetrates primary AML cells (AML3639, AML CP, AML0932), while shows extremely low uptake in primary colon adenocarcinoma cells and NHDF^[1].
The cellular uptake of CPP44 (2 μM; 3 h) into AML cells can be blocked by Dynasore (HY-15304) (80 μM; 1 h pretreatment), whereas EIPA (HY-101840) and Chlorpromazine (HY-12708) exert no significant inhibitory effect on its uptake; uptake of CPP44 is blocked at 4°C, indicating that it mainly enters cells via an ATP-dependent, dynamin-dependent, and clathrin-independent endocytic pathway^[1].
Uptake of CPP44 (2 μM; 3 h) decreases significantly in myeloid leukemia cells with M160 (CD163L1) siRNA (50 nM)-mediated knockdown; knockdown of M160 in HepG2 cells also reduces CPP44 uptake, supporting the involvement of M160 in tumor-selective internalization of CPP44^[1].
CPP44 enables active targeting of CPDS nanoparticles to THP-1 AML cells, which is confirmed by the reduction of intracellular fluorescence signals after competitive pretreatment with free CPP44 peptides^[2].
FITC-labelled CPP44 (10 μM) exhibits poor penetration into non-tumorigenic PBMC^[1].

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