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9-Aminocamptothecin
9-Aminocamptothecin
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name 9-Aminocamptothecin
Price: $128 / 20mg
CAS No.: 91421-43-1
Catalog No.: CFN90309
Molecular Formula: C20H17N3O4
Molecular Weight: 363.37 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Source: The barks of Camptotheca acuminata Decne
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
Size /Price /Stock 10 mM * 1 mL in DMSO / $46.0 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: 9-Aminocamptothecin is a topoisomerase I inhibitor with potent anticancer activity.In combination with 9-Aminocamptothecin, one 15-mer peptide (SAYAATVRGPLSSAS) has synergistic cytotoxic effects with 9-Aminocamptothecin both in the cytotoxicity assay and in nude mouse xenograft human tumor models.
Targets: P450 (e.g. CYP17)
In vitro:
Int J Oncol. 2014 Aug;45(2):877-86.
Cytochrome P450 3A-mediated metabolism of the topoisomerase I inhibitor 9-aminocamptothecin: impact on cancer therapy.[Pubmed: 24889073]
The metabolism of 9-Aminocamptothecin (9-AC) was investigated in human and rat liver microsomes.
METHODS AND RESULTS:
In both species 9-Aminocamptothecin was almost exclusively biotransformed to dihydroxy-9-Aminocamptothecin (M1) and monohydroxy-9-Aminocamptothecin (M2). The enzymatic efficiencies of the formation of M1 and M2 (V(max)/K(m)) were 1.7- and 2.7‑fold higher in rat than in human liver microsomes indicating species-related differences in 9-Aminocamptothecin hydroxylation. Incubation in the presence of human recombinant cytochrome P450 (CYP) enzymes demonstrated that the formation of M1 and M2 is mainly catalyzed by CYP3A4 and only to a minor extent by extrahepatic CYP1A1. The predominant role of CYP3A4 was further supported by a dramatic inhibition of metabolite formation in the presence of the CYP3A4 substrates troleandomycin and ketoconazole. Experiments conducted in isolated perfused rat livers further demonstrated that biliary excretion of 9-Aminocamptothecin, M1 and M2 during 60 min of perfusion was pronounced and accounted for 17.7±2.59, 0.05±0.01 and 2.75±0.14% of total 9-Aminocamptothecin applied to the liver, respectively.
CONCLUSIONS:
In summary, this study established that CYP3A-dependent hydroxylation is the main metabolic pathway for 9-Aminocamptothecin in rat and human liver, which have to be taken into consideration during cancer therapy of patients.
In vivo:
Macromol Biosci. 2009 Nov 10;9(11):1135-42.
Antitumor efficacy of colon-specific HPMA copolymer/9-aminocamptothecin conjugates in mice bearing human-colon carcinoma xenografts.[Pubmed: 19685500 ]
The antitumor activity of a colon-specific N-(2-hydroxypropyl)methacrylamide (HPMA) copolymer - 9-Aminocamptothecin (9-AC) conjugate (P-9-AC) was assessed in orthotopic and subcutaneous animal (HT29 xenograft) tumor models.
METHODS AND RESULTS:
P-9-AC treatment of mice bearing orthotopic colon tumors, with a dose of 3 mg/kg of 9-AC equivalent every other day for 6 weeks, resulted in regression of tumors in 9 of 10 mice. A lower dose of P-9-AC (1.25 mg/kg of 9-AC equivalent) every other day for 8 weeks inhibited subcutaneous tumor growth in all mice. No liver metastases were observed.
CONCLUSIONS:
Colon-specific release of 9-AC from polymer conjugates enhanced antitumor activity and minimized the systemic toxicity.
Cancer Chemother Pharmacol. 2009 Apr;63(5):793-8.
Phase II study of 9-aminocamptothecin in previously treated lymphomas: results of Cancer and Leukemia Group B 9551.[Pubmed: 18648813]
To evaluate the efficacy and toxicity of the topoisomerase I inhibitor, 9-Aminocamptothecin (9-AC), in patients with relapsed lymphoma and to correlate 9-AC plasma concentrations with response and toxicity.
METHODS AND RESULTS:
Eligible patients had relapsed Hodgkin lymphoma (HL) treated with one or two prior regimens, low grade non-Hodgkin's lymphoma (NHL) treated with one or two prior regimens, or aggressive NHL treated with one prior regimen. The first nine patients received 9-AC dimethylacetamide 0.85 mg/m(2) per day intravenously over 72 h every 2 weeks and the remaining 27 patients received 9-AC/colloidal dispersion 1.1 mg/m(2) per day. Patients received a minimum of three cycles unless progression or intolerable toxicity occurred. Responding patients received two cycles past best response with a minimum of six cycles. CALGB 9551 accrued 37 patients from April 1996 through October 2000; one patient with HD, 18 patients with indolent lymphoma, and 17 patients with aggressive lymphoma. The overall response rate was 17%, with response rates of 11% (2 partial responses) in patients with indolent histologies and 23% (1 complete response, 3 partial responses) in patients with aggressive histologies. The patient with HD did not respond. Response rates were similar for both drug formulations. The median remission duration for the six responders was 6.5 months, with one remission lasting longer than 12 months. Significant grade 3 and 4 toxicities included neutropenia (66%), anemia (31%), and thrombocytopenia (36%), with 20% of patients experiencing grade 3 or 4 infection. No treatment related deaths occurred. Steady state serum concentrations did not correlate with patient response or toxicity.
CONCLUSIONS:
Single agent 9-AC has modest activity in aggressive non-Hodgkin's lymphomas.
9-Aminocamptothecin Description
Source: The barks of Camptotheca acuminata Decne
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: 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.

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After receiving: 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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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.752 mL 13.7601 mL 27.5202 mL 55.0403 mL 68.8004 mL
5 mM 0.5504 mL 2.752 mL 5.504 mL 11.0081 mL 13.7601 mL
10 mM 0.2752 mL 1.376 mL 2.752 mL 5.504 mL 6.88 mL
50 mM 0.055 mL 0.2752 mL 0.5504 mL 1.1008 mL 1.376 mL
100 mM 0.0275 mL 0.1376 mL 0.2752 mL 0.5504 mL 0.688 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Mol Cancer Ther. 2006 Mar;5(3):739-45.
Identification of a small topoisomerase I-binding peptide that has synergistic antitumor activity with 9-aminocamptothecin.[Pubmed: 16546989]
The topoisomerase I (top1)-targeted camptothecin class of anticancer drugs is important in the treatment of several types of cancers. This class of drug inhibits the top1 enzyme during its catalytic DNA relaxation cycle, stabilizing the transient covalent top1-DNA complex by simultaneous noncovalent interactions with DNA and top1.
METHODS AND RESULTS:
We examined top1 using phage display because of the significance of this known top1-directed drug action. Several peptides that bind top1 were discovered and these were examined for top1 affinity, top1 catalytic and cleavage complex effects, and cytotoxic effects in cultured cell lines and in an in vivo tumor model. Although several peptides exhibited nanomolar and low-micromolar affinity for top1, none had cytotoxic effects when administered alone.
CONCLUSIONS:
However, in combination with 9-Aminocamptothecin, one 15-mer peptide (SAYAATVRGPLSSAS) had synergistic cytotoxic effects with 9-Aminocamptothecin both in the cytotoxicity assay and in nude mouse xenograft human tumor models. This report details the investigation of this peptide.
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