SN-38 - CAS 86639-52-3

SN-38 - CAS 86639-52-3 Catalog number: BADC-00841

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SN-38 (NK012) is an active metabolite of the Topoisomerase I inhibitor Irinotecan. SN-38 (NK012) inhibits DNA and RNA synthesis with IC50s of 0.077 and 1.3 μM, respectively.

ADCs Cytotoxin
Product Name
Catalog Number
Molecular Formula
Molecular Weight
392.40 g/mol

Ordering Information

Catalog Number Size Price Quantity
BADC-00841 1 g $198
SN-38 (NK012) is an active metabolite of the Topoisomerase I inhibitor Irinotecan. SN-38 (NK012) inhibits DNA and RNA synthesis with IC50s of 0.077 and 1.3 μM, respectively.
Canonical SMILES
1.51 g/cm3
DMSO: 25 mg/ml (ultrasonic), H2O: < 01 mg/ml
Melting Point
>185 ℃
Mechanism Of Action
The entrapment of SN-38 in lipsomes results in a more stable and more soluble form of the drug. This allows for increased affinity of SN-38 to lipid membranes and improved delivery of the drug to tumor sites. SN-38 is a highly effective cytotoxic topoisomerase I inhibitor.
SN-38 (7-ethyl-10-hydroxycamptothecin) is the active metabolite of Irinotecan (CPT-11). Irinotecan is a topoisomerase I inhibitor commercially available as Camptosar®. SN-38 has been found to be 200-2000 times more cytotoxic than CPT-11, but has not been used as an anticancer drug due to its poor solubility in pharmaceutically acceptable solvents and low affinity to lipid membranes. SN-38 also undergoes a reversible conversion to an inactive open lactone ring structure at physiological pH. LE-SN-38 is a novel lipsome based formulation containing liposomes of uniform size distribution (<200 nm). Drug entrapment efficiency of the formulation is>95%.
Clinical Trial Information
NCT NumberCondition Or DiseasePhaseStart DateSponsorStatus
NCT03824899Locally Advanced Rectal CancerNot Applicable2019-01-31Fudan UniversityUnknown Verified January 2019 by Zhu Ji, Fudan University. Recruitment status was Recruiting
NCT01251926NeoplasmsPhase 12019-11-15National Cancer Institute (NCI)Completed
NCT02662959Stomach NeoplasmsPhase 22016-01-26Fudan UniversityUnknown Verified November 2015 by Weijian Guo, Fudan University. Recruitment status was Recruiting
NCT00311610Colorectal CancerPhase 22016-06-29Alliance for Clinical Trials in OncologyCompleted
NCT04209595Small Cell Lung CancerPhase 1, Phase 22021-09-29National Cancer Institute (NCI)Suspended (Pending approval of amendment)
the treatment of colorectal cancer
White solid powder
99.4 %
Room temperature, or blue ice upon request.
-20 ℃
Acute Toxic; Health Hazard
Signal Word
Boiling Point
810.3 ℃ at 760 mmHg
1.Predictive effects of bilirubin on response of colorectal cancer to irinotecan-based chemotherapy.
Yu QQ1, Qiu H1, Zhang MS1, Hu GY1, Liu B1, Huang L1, Liao X1, Li QX1, Li ZH1, Yuan XL1. World J Gastroenterol. 2016 Apr 28;22(16):4250-8. doi: 10.3748/wjg.v22.i16.4250.
AIM: To examine the predictive effects of baseline serum bilirubin levels and UDP-glucuronosyltransferase (UGT) 1A1*28 polymorphism on response of colorectal cancer to irinotecan-based chemotherapy.
2.A Randomized, Phase II Trial of Cetuximab With or Without PX-866, an Irreversible Oral Phosphatidylinositol 3-Kinase Inhibitor, in Patients With Metastatic Colorectal Carcinoma.
Bowles DW1, Kochenderfer M2, Cohn A3, Sideris L4, Nguyen N5, Cline-Burkhardt V6, Schnadig I7, Choi M8, Nabell L9, Chaudhry A10, Ruxer R11, Ucar A12, Hausman D13, Walker L13, Spira A14, Jimeno A15. Clin Colorectal Cancer. 2016 Mar 31. pii: S1533-0028(16)30029-9. doi: 10.1016/j.clcc.2016.03.004. [Epub ahead of print]
BACKGROUND: The phosphotidylinositol-3 kinase (PI3K)/serine-threonine kinase/mammalian target of rapamycin signaling pathway is frequently altered in colorectal cancer (CRC). PX-866 is an oral, irreversible, pan-isoform inhibitor of PI3K. This randomized phase II study evaluated cetuximab with or without PX-866 in patients with metastatic, anti-epidermal growth factor receptor-naive, KRAS codon 12 and 13 wild-type CRC.
3.Effect of Single Nucleotide Polymorphisms in the Xenobiotic-sensing Receptors NR1I2 and NR1I3 on the Pharmacokinetics and Toxicity of Irinotecan in Colorectal Cancer Patients.
Mbatchi LC1,2,3, Robert J4, Ychou M2,5, Boyer JC1, Del Rio M2, Gassiot M1,2, Thomas F6, Tubiana N7, Evrard A8,9,10. Clin Pharmacokinet. 2016 Apr 26. [Epub ahead of print]
BACKGROUND AND OBJECTIVES: Nuclear receptors PXR (pregnane X receptor, NR1I2) and CAR (constitutive androstane receptor, NR1I3) are key regulators of irinotecan metabolism, and ligand-dependent modulation of their activity leads to significant drug-drug interactions. Because genetic polymorphisms can also affect the activity of these xenobiotic-sensing receptors, we hypothesized that they could contribute to the interpatient variability of irinotecan pharmacokinetics and to the toxicity of irinotecan-based regimens.
4.The contribution of pharmacogenetics to pharmacovigilance.
Bondon-Guitton E1, Despas F2, Becquemont L3. Therapie. 2016 Mar-Apr;71(2):223-8. doi: 10.1016/j.therap.2016.02.005. Epub 2016 Mar 3.
Since the beginning of this century, information on pharmacogenetics appears in the summary of product characteristics (SPC) of drugs. Pharmacogenetic tests particularly concern the enzymes involved in the metabolism of drugs, among which P450 cytochromes. Some patients known as poor metabolisers eliminate some drugs more slowly, causing overdoses and adverse drug reactions (ADRs). The best-known examples are AVK and VKORC1-CYP2C9 or clopidogrel and CYP2C19. In the USA, the tests are recommended before the introduction of these drugs to prevent the occurrence of ADRs. Other tests are also commonly performed to address the toxicity of certain anticancer drugs (DPYD-capecitabine, UGT1A1-irinotecan, TPMT 6-mercaptopurine). Pharmacogenetic testing is also available to identify HLA loci that are very strongly associated with the occurrence of immuno-allergic reactions to a specific drug. The best-known example is HLA-B*5701, strongly associated with hypersensitivity to abacavir, and this test is now always prescribed before the instatement of this drug.

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