Camptothecin

Camptothecin
Product Name Camptothecin
CAS No.: 7689-03-4
Catalog No.: CFN97249
Molecular Formula: C20H16N2O4
Molecular Weight: 348.4 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Targets: Beta Amyloid | p53 | IL Receptor | Topoisomerase
Source: The barks of Camptotheca acuminata Decne.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Price: $30/20mg
Camptothecin is a specific inhibitor of DNA topoisomerase I (Topo I) with IC50 of 0.68 μM; it is a novel alkaloidal leukemia and tumor inhibitor, is a strong inhibitor of nucleic acid synthesis in mammalian cells and a potent inducer of strand breaks in chromosomal DNA. Camptothecin and its analogs reduce amyloid-β production and amyloid-β42-induced IL-1β production.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    J Alzheimers Dis. 2015;43(2):465-77.
    Camptothecin and its analogs reduce amyloid-β production and amyloid-β42-induced IL-1β production.[Pubmed: 25096614]
    Compounds derived from natural products are becoming promising alternative drugs/tools in Alzheimer's disease (AD) therapeutics.
    METHODS AND RESULTS:
    From an in-house natural products library, seventeen hits were selected for their inhibitory effect on the production of amyloid-β (Aβ) with IC50 lower than 10 μM without causing obvious toxicity. Among these compounds, Camptothecin (CPT) and its analogs showed inhibitory effects on amyloid-β 1-42 (Aβ42) with the IC50 value in the nanomolar range in HEKsw cells and SHSY5Ysw cells. Further studies showed that CPT and its analogs inhibited Aβ42 via a p53 dependent pathway. Meanwhile, CPT and its analogs could also inhibit Aβ42 induced IL-1β production in the THP-1 cells.
    CONCLUSIONS:
    Taken together, our results indicate that CPT and its analogs would be a promising therapeutic candidates for AD.
    J Drug Target. 2014 Dec;22(10):913-26.
    Development and evaluation of magnetic microemulsion: tool for targeted delivery of camptothecin to BALB/c mice-bearing breast cancer.[Pubmed: 25119147]
    Development and evaluation of Camptothecin-loaded-microemulsion (ME) and -magnetic microemulsion (MME) for passive/active-targeted delivery to BALB/c mice-bearing breast cancer.
    METHODS AND RESULTS:
    Based on the pseudo-ternary phase diagrams Camptothecin-loaded-MEs and -MMEs were developed using benzyl alcohol:Captex 300 (3:1), TPGS:Tween 80 (2:1) and water. Furthermore, characterized for their droplet size distribution, magnetic susceptibility and effect of droplet size in plasma and evaluated for in vitro and in vivo targeting potential, drug release, haemolytic potential, cytotoxicity, genotoxicity, in vivo biodistribution and lactone ring stability. Drug-loaded MEs showed uniform droplet distribution, extended drug release (76.07 ± 4.30% at 24 h), acceptable level of haemolytic activity (<20%), significant cytotoxicity (129 ± 3.9 ng/mL) against MCF-7 cancer cells and low DNA damage in lymphocytes. Targeting potential of MMEs was documented in 4T1 breast cancer-induced BALB/c mice. MMEs were concentrated more at the target tissue on introduction of external magnetic field. In vivo biodistribution study documented the active targeting of 5067.56 ± 354.72 ng/gm and passive targeting of 1677.58 ± 134.20 ng/gm Camptothecin to breast cancer from MME and ME, respectively. Lactone stability study shows around 80% of the lactone stable at 24 h.
    CONCLUSIONS:
    Developed ME and MME may act as a promising nanocarrier for efficient targeting of breast cancer tissues.
    Nanomedicine. 2014 Oct;10(7):1477-86.
    Pharmacodynamic and pharmacogenomic study of the nanoparticle conjugate of camptothecin CRLX101 for the treatment of cancer.[Pubmed: 24768630]
    CRLX101 is a nanopharmaceutical consisting of cyclodextrin-based polymer molecule and Camptothecin. The CRLX101 nanoparticle is designed to concentrate and slowly release Camptothecin in tumors over an extended period of time.
    METHODS AND RESULTS:
    Tumor biopsy and blood samples collected from patients with advanced solid malignancies before and after CRLX101 treatment are subjected to immunohistochemistry and pharmacogenomics. The expression of Topoisomerase-1, Ki-67, CaIX, CD31 and VEGF decreased after CRLX101 treatment. The expressions of these proteins are inversely proportional with survival duration of the patients. The Drug Metabolism Enzymes and Transporters (DMET) array shows an allele frequency in patients similar to global populations with none of the SNPs associated with toxicity. The results suggest that the observed lower toxicity is not likely to be due to different genotypes in SNPs. CRLX101 demonstrates a promising anti-tumor activity in heavily pre-treated or treatment-refractory solid tumor malignancies presumably by inhibition of proliferation and angiogenesis correlating with tumor growth inhibition. From the clinical editor: In this cancer treatment study clinical samples collected from patients were subjected to immunohistochemistry and pharmacogenomics.
    CONCLUSIONS:
    The expressions of key proteins that are inversely proportional with survival duration of the patients decreased after treatment with CRLX101, a Camptothecin slow-release nanoparticle conjugate. This anti-tumor activity in heavily pre-treated and treatment resistant solid tumors, promises a novel therapeutic approach.
    J Biol Chem. 1985 Nov 25;260(27):14873-8.
    Camptothecin induces protein-linked DNA breaks via mammalian DNA topoisomerase I.[Pubmed: 2997227]
    Camptothecin, a cytotoxic drug, is a strong inhibitor of nucleic acid synthesis in mammalian cells and a potent inducer of strand breaks in chromosomal DNA.
    METHODS AND RESULTS:
    Neither the equilibrium dialysis nor the unwinding measurement indicates any interaction between Camptothecin and purified DNA. However, Camptothecin induces extensive single strand DNA breaks in reactions containing purified mammalian DNA topoisomerase I. DNA breakage in vitro is immediate and reversible. Analyses of Camptothecin-induced DNA breaks show that topoisomerase I is covalently linked to the 3' end of the broken DNA. In addition, Camptothecin inhibits the catalytic activity of mammalian DNA topoisomerase I. We propose that Camptothecin blocks the rejoining step of the breakage-reunion reaction of mammalian DNA topoisomerase I. This blockage results in the accumulation of a cleavable complex which resembles the transient intermediate proposed for eukaryotic DNA topoisomerase I.
    CONCLUSIONS:
    The inhibition of nucleic acid synthesis and the induction of DNA strand breaks observed in vivo may be related to the formation of this drug-induced cleavable complex.
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