CPP44
CPP44 is a tumor lineage-homing cell-penetrating peptide (CPP) that selectively enters myeloid leukemia cells and liver tumor cells. The cellular internalization of CPP44 is associated with M160 (CD163L1), and it mainly enters cells via an ATP- and dynein-dependent, clathrin-independent endocytic pathway. CPP44 can be used in studies related to acute myeloid leukemia, hepatocellular carcinoma, tumor-targeted delivery, and tumor imaging.
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- CAS No.: 934965-51-2
- 화학식: C91H142N28O20S2
- 분자량:2012.41
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보관:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocol
- 순도&문서
- References
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Help & FAQs
Biological Activity
제품 설명
In Vitro
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. Further protocols information, click here.
In Vivo
CPDS nanoparticles containing CPP44 (siRNA: 1.0 mg/kg; DNR: 0.32 mg/kg; i.v.) show significantly greater enrichment in AML-infiltrated liver and spleen compared to free siRNA in the THP-1-Luc/T-cell humanized NOG AML model, supporting the application of CPP44 in targeted delivery for AML[2].
CPP44-PEG@IRMOF-1 (i.v.) shows significant tumor enrichment starting at approximately 6 h in HepG2 tumor-bearing nude mice. At 24 h, its accumulation in tumors is higher than that of unmodified IRMOF-1, while its accumulation in normal liver tissues is relatively reduced, which supports that CPP44 enhances liver tumor targeting and tissue penetration[4].
PPCi nanoparticles containing CPP44RPM (siRNA: 1 mg/kg; tail vein injection) exhibit tumor-targeted accumulation in HepG2-luc xenograft BALB/c nude mice; siPLK1@PPC containing CPP44RPM (siRNA: 1 mg/kg; intratumoral injection; every other day; 20 days) can persistently retain in tumors and reduce tumor volume and weight, and this result belongs to the CPP44-functionalized derivative delivery system[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude mice (female, ~20 g, hepatocellular carcinoma xenograft model)[4]
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Dosage:1 mg/kg siRNA
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Administration:intratumoral injection; every other day; 20 days
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Result:Reduced final tumor weight by >50% compared to PBS controls.
Downregulated PLK1 mRNA expression in tumor tissue by over 50% relative to PBS controls.
Prolonged mouse survival significantly compared to control groups.
Maintained stable mouse body weight throughout the study period.
Induced greater tumor tissue damage and apoptosis than sorafenib, with no obvious systemic toxicity to major organs.
Chemical Information
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CAS No. 934965-51-2
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분자량 2012.41
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화학식 C91H142N28O20S2
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Sequence
Lys-Arg-Pro-Thr-Met-Arg-Phe-Arg-Tyr-Thr-Trp-Asn-Pro-Met-Lys
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Sequence Shortening
KRPTMRFRYTWNPMK
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선적
Room temperature in continental US; may vary elsewhere.
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보관
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocol
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Liver Cancer Modeling
Liver cancer can be classified into primary liver cancer and secondary liver cancer. Secondary liver cancer is the metastatic liver cancer. Primary liver cancer includes hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC) and fibrolamellar HCC, of which HCC is the most common form, accounting for approximately 90% of primary liver cancers[1]. HCC mouse models include chemical agent-induced models, transplanted tumor models, and genetic engineered models.
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Bioluminescent/Fluorescent Imaging Xenograft
Bioluminescent and fluorescent imaging xenograft models use tumor cells engineered to express optical reporters so tumor engraftment, growth, dissemination, and treatment response can be monitored longitudinally in living animals and validated ex vivo. Bioluminescence imaging usually measures luciferase activity after substrate administration and is commonly used as a surrogate for viable reporter-expressing tumor burden, while fluorescence imaging measures reporter or probe emission and can support tumor localization, ex vivo confirmation, or complementary multimodal analysis.
순도&문서
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
CPP44 Related Classifications
HY-P11925 Related Classifications
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