Camptothecin (CPT)

Catalog No.S1288 Batch:S1288

Print

Technical Data

Formula

C20H16N2O4
Molecular Weight 348.35 CAS No. 7689-03-4
Solubility (25°C)* In vitro DMSO 3 mg/mL (8.61 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 A specific inhibitor of DNA topoisomerase I (Topo I) with IC50 of 0.68 μM in a cell-free assay, Camptothecin (CPT) 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 (CPT), a plant alkaloid originally isolated from *Camptotheca acuminata* in 1966,[1] is noted to halt cells during the S phase of mitosis. It 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, this compound induces apoptosis in primary mouse hepatocytes, with an IC50 value of 13 μM. It also abrogates 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, CPT (5 μM) induces proteasome-mediated degradation of mixed lineage leukemia 5 (MLL5) protein, which leads to phosphorylation of p53 at Ser392.[5] Due to its low solubility and adverse effects, various analogues have been developed, and two of them, topotecan and irinotecan, have been approved by the FDA and are used in cancer chemotherapy.
In vivo Camptothecin (CPT) (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 this compound (50 mg/kg) and TNF (5 and 7 μg/kg), but not it 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. This compound 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 obtained.
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 (CPT) for 48 hours and then with fresh medium for 48 hours. This compound 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

References

  • http://pubs.acs.org/doi/abs/10.1021/ja00968a057
  • https://pubmed.ncbi.nlm.nih.gov/7853331/
  • https://pubmed.ncbi.nlm.nih.gov/2032244/
  • https://pubmed.ncbi.nlm.nih.gov/15122760/
  • https://pubmed.ncbi.nlm.nih.gov/21423215/

Customer Product Validation

Growth suppression by UBE2M silencing is enhanced by DNA damaging agents. Growth sensitivity of HEY cells in the presence of Camptothecin(CPT) was monitored using clonogenic assay.

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

<p>CtIP and exonuclease 1 protect cells from chromosomal damage. (<strong>A</strong>) At 72 h after transfection with the indicated siRNA oligonucleotides, U2OS cells were treated with either DMSO or camptothecin (1 h, 1 μM; acute treatment) and survival was determined by colony formation. Data represent the mean±s.e.m. of five independent experiments. (<strong>B</strong>) Cell survival at low doses of camptothecin from the data shown in (<strong>A</strong>). Data represent the mean±s.e.m. of five independent experiments. (<strong>C</strong>) Cells transfected as in (<strong>A</strong>) were treated with either DMSO or camptothecin for 24 h (chronic treatment) and survival was determined by colony formation. Data represent the mean±s.e.m. of three independent experiments. (<strong>D</strong>) Metaphase spreads from cells transfected and treated as described in (<strong>A</strong>) were analysed for chromosomal aberrations. A total of 50 metaphase spreads was analysed for each sample. The percentages of metaphase spreads displaying the indicated numbers of radial chromosomes are shown. CNTL, control; DMSO, dimethyl sulphoxide; EXO1, exonuclease 1; siRNA, small interfering RNA.</p>

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

<p>U2OS cells transfected with siRNA oligonucleotides were treated with DMSO or camptothecin (1 μM, 1 h) and DNA-PKcs autophosphorylation at S2056 was monitored. Arrow indicates the hyperphosphorylated form of CtIP.</p>

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

a. Effects of five concentrations of CXCL12 (0, 10, 50, 100, and 500 ng/ml) on apoptosis of NPC cells caused by 10 μM camptothecin were determined by the amount of cleaved PARP detected by Western blot.

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

Selleck's Camptothecin (CPT) Has Been Cited by 169 Publications

Non-canonical functions of DNMT3A in hematopoietic stem cells regulate telomerase activity and genome integrity [ Cell Stem Cell, 2025, S1934-5909(25)00256-5] PubMed: 40680747
Inherited deficiency of DIAPH1 identifies a DNA double strand break repair pathway regulated by γ-actin [ Nat Commun, 2025, 16(1):4491] PubMed: 40368919
A novel biosensor for the spatiotemporal analysis of STING activation during innate immune responses to dsDNA [ EMBO J, 2025, 10.1038/s44318-025-00370-y] PubMed: 39984755
DSCC1 restrains 53BP1/RIF1 signaling at DNA double-strand breaks to promote homologous recombination repair [ Cell Rep, 2025, 44(4):115452] PubMed: 40117291
Steroid-Modulated Transcription Synergistically Forms DNA Double-Strand Breaks With Topoisomerase II Inhibitor [ Cancer Sci, 2025, 10.1111/cas.70081] PubMed: 40231641
The novel role of LCK and other PcDEGs in the diagnosis and prognosis of sepsis: Insights from bioinformatic identification and experimental validation [ Int Immunopharmacol, 2025, 149:114194] PubMed: 39904039
The Kinase Inhibitor GNF-7 Is Synthetically Lethal in Topoisomerase 1-Deficient Ewing Sarcoma [ Cancers (Basel), 2025, 17(15)2475] PubMed: 40805174
Peroxiredoxin 1 inhibits tumorigenesis by activating the NLRP3/GSDMD pathway to induce pyroptosis of colorectal cancer cells [ World J Gastroenterol, 2025, 31(36):111557] PubMed: 41025079
Discovery and Characterization of Small Molecule Inhibitors Targeting Exonuclease 1 for Homologous Recombination-Deficient Cancer Therapy [ ACS Chem Biol, 2025, 10.1021/acschembio.5c00117] PubMed: 40378357
DDX18 influences chemotherapy sensitivity in colorectal cancer by regulating genomic stability [ Exp Cell Res, 2025, 444(1):114344] PubMed: 39577603

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.