Camptothecin (CPT)

Catalog No.S1288 Batch:S128809

Print

Technical Data

Formula

C20H16N2O4
Molecular Weight 348.35 CAS No. 7689-03-4
Solubility (25°C)* In vitro DMSO 4 mg/mL (11.48 mM)
Water Insoluble
Ethanol Insoluble
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Camptothecin (CPT) is a specific inhibitor of DNA topoisomerase I (Topo I) with IC50 of 0.68 μM in a cell-free assay. Camptothecin induces apoptosis in cancer cells via microRNA-125b-mediated mitochondrial pathways. Phase 2.
Targets
Topo I [2]
(Cell-free assay)
0.68 μM
In vitro Camptothecin, a plant alkaloid orignially isolated from Camptotheca acuminate in 1966. [1] Camptothecin is noted to halt cells during the S phase of mitosis. Camptothecin displays nanomolar potency in cytotoxicity against many human tumor cell lines, including HT29, LOX, SKOV3, and SKVLB, with IC50 values ranging from 37 nM to 48 nM. [2] In combination with TNF, Camptothecin induces apoptosis in primary mouse hepatocytes, with an IC50 value of 13 μM. Camptothecin also abrogated the TNF-induced NF-κB Activation, as well as the expression of TNF-receptor associated factor 2 (TRAF2), X-linked inhibitor of apoptosis protein (X-IAP), and FLICE-inhibitory protein (FLIP). [4] In HCT116 cells, Camptothecin (5 μM) induces proteasome-mediated degradation of mixed lineage leukemia 5 (MLL5) protein, which leads to phosphorylation of p53 at Ser392. [5] Due to the low solubility and adverse effects of Camptothecin, various Camptothecin analogues have been developed, and two of them, topotecan and irinotecan, has been approved by FDA and are used in cancer chemotherapy.
In vivo Camptothecin (8 mg/kg) displays complete growth inhibition and regression in mice xenografts of various tumors, including colon, lung, breast, stomach, and ovary tumors. [3] In mice, combinations of Camptothecin (50 mg/kg) and TNF (5 and 7 μg/kg), but not Camptothecin alone, induces liver damage. [4]

Protocol (from reference)

Kinase Assay:[2]
  • Topoisomerase I Cleavable Complex Assay

    Topoisomerase I is isolated from calf thymus and is devoid of topoisomerase II. All reactions are carried out in 10 mL volumes of reaction buffer (50 mM Tris-HCl, pH 7.5, 100 mM KCl, 0.5 mM EDTA, and 30 pg/mL BSA) in microtiter plates. Camptothecin is dissolved in DMSO at 10 mg/mL and serially diluted in 96-well microtiter plates to which the 32P end-labeled pBR322 DNA and topoisomerase enzyme are added. The reaction mixture is incubated at room temperature for 30 min and then the reaction stopped by adding 2 mL of a mixture of sodium dodecyl sulfate and proteinase K (1.6% and 0.14 mg/mL final concentrations, respectively). The plates are heated at 50 °C for 30 min, 10 mL of standard stop mixture containing 0.45 N NaOH is added in order to generate single-stranded DNA, and the samples are electrophoresed in 1.5% agarose gels in TBE buffer. Gels are blotted on nitrocellulose paper, dried, and exposed to X-ray film. The units of cleavage are calculated from the autoradiographs and plotted against the log drug concentration. The IC50 values are then obtaine
Cell Assay:[2]
  • Cell lines

    U87MG, A549 and H838 cells

  • Concentrations

    0.17 nM–10 mM

  • Incubation Time

    48 hours

  • Method

    Tumor cells are plated in 100 μL of medium in 96-well microtiter plates at a density of 1500 to 4000 cells per well and allowed to adhere overnight. Cells are incubated with Camptothecin for 48 hours and then with fresh medium for 48 hours. Camptothecin at each concentration is added in quadruplicate. Following a 4-hour incubation of treated cells with MTT, the reduced dye product is extracted from the cells with 0.2 mL of DMSO followed by 50 μL of Sorensen's buffer. The plates are shaken briefly, and the absorbance at 570 nm is read and quantitated. Curves are fitted to the MTT assay data using a four-parameter logistic equation.
Animal Study:[3]
  • Animal Models

    Nude mice (NIH-I high fertility strain) bearing xenografts of CASE, SW48, DOY, SPA, and CLO cells

  • Dosages

    0–8 mg/kg

  • Administration

    Administered via i.m. or i.v. injection

Customer Product Validation

Data from [Data independently produced by PLoS One, 2014, 9(7), e101844]

Data from [EMBO Rep, 2010, 11(12), 962-8]

Data from [EMBO Rep, 2010, 11(12), 962-8]

Data from [Data independently produced by , , Tumour Biol, 2016, 37(6):8169-79]

Selleck's Camptothecin (CPT) has been cited by 151 publications

H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours [ Nat Commun, 2024, 15(1):4430] PubMed: 38789420
SIRT1 ISGylation accelerates tumor progression by unleashing SIRT1 from the inactive state to promote its deacetylase activity [ Exp Mol Med, 2024, 56(3):656-673] PubMed: 38443596
Human PC4 supports telomere stability and viability in cells utilizing the alternative lengthening of telomeres mechanism [ EMBO Rep, 2024, ] PubMed: 39468351
Dual targeting of the androgen receptor and PI3K/AKT/mTOR pathways in prostate cancer models improves antitumor efficacy and promotes cell apoptosis [ Mol Oncol, 2024, 10.1002/1878-0261.13577] PubMed: 38225213
Metachromin C, a marine-derived natural compound, shows potential in antitumor activity [ Int J Med Sci, 2024, 21(13):2578-2594] PubMed: 39439453
Epigenetic targeting of PGBD5-dependent DNA damage in SMARCB1-deficient sarcomas [ bioRxiv, 2024, 2024.05.03.592420] PubMed: 38766189
NRDE2 deficiency impairs homologous recombination repair and sensitizes hepatocellular carcinoma to PARP inhibitors [ Cell Genom, 2024, 4(5):100550] PubMed: 38697125
RAD51C-XRCC3 structure and cancer patient mutations define DNA replication roles [ Nat Commun, 2023, 14(1):4445] PubMed: 37488098
SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance [ Nat Commun, 2023, 14(1):3034] PubMed: 37236926
SMARCB1 regulates a TFCP2L1-MYC transcriptional switch promoting renal medullary carcinoma transformation and ferroptosis resistance [ Nat Commun, 2023, 14(1):3034] PubMed: 37236926

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.