Irinotecan HCl Trihydrate

Catalog No.S2217 Synonyms: CPT-11 HCl Trihydrate

Irinotecan HCl Trihydrate Chemical Structure

Molecular Weight(MW): 677.18

Irinotecan prevents DNA from unwinding by inhibition of topoisomerase 1.

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In DMSO USD 190 In stock
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Cited by 13 Publications

4 Customer Reviews

  • Growth inhibitory effects of Irinotecan in human pancreatic cancer cells. Panc1 cells were plated in triplicates into 48-well plates at a density of 10,000 cells/ml. After 24 hours, complete culture medium was changed into fresh low-serum-containing medium (1% FBS) containing DMSO (control) or indicated doses of Irinotecan (Selleckchem). Cell viability 72 hours after treatment was determined by AlamarBlue assay (Invitrogen) according to manufacturer's instructions. Results are expressed as percentages of control, which was arbitrarily assigned 100% viability, and represented as the mean ± standard deviation (SD) of the tripicate wells. 

    Dr. Mikhail Menshikov of Cardiology Research Center. Irinotecan HCl Trihydrate purchased from Selleck.

  • In vitro cell uptake data showing the HA coating on HAC-PFP-DC nanoparticles significantly improves drug delivery into prostasphere and mammosphere cells enriched with CSCs. Fluorescence micrographs of (A) prostasphere and (B) mammosphere cells after incubated with the simple mixture of free DOX&CPT, PFP-DC nanoparticles, and HAC-PFP-DC nanoparticles for 3 h at 37 °C. CPT:irinotecan

    Biomaterials, 2015, 72:74-89. Irinotecan HCl Trihydrate purchased from Selleck.

  • Monolayer cultures of human OVCAR-5 cells were incubated with Mn, irinotecan or their combination for 6, 24, and 48 hours. Representative immunofluorescence imaging of Tdp1 (red fluorescence) and γH2AX (green fluorescence) in OVCAR-5 cells subjected to (i) No-treatment (NT); (ii) Mn ; (iii) Irinotecan; and (iv) Combination of Mn and irinotecan for 24 hours.

    Mol Cancer Ther, 2018, 17(2):508-520. Irinotecan HCl Trihydrate purchased from Selleck.

  • (A) HCT116 and (B) HT29 cells were cultured with 0.1% DMSO (control) or A452 (0.5, 1, 2 uM), SAHA (5 uM), cisplatin (10 uM), irinotecan (5 uM), or capecitabine (10 uM) at the indicated concentrations for 24 h. The Western blot analysis shows PARP degradation, proapoptotic and antiapoptotic markers. α-Tubulin is shown as a loading control.

    Carcinogenesis, 2018, 39(1):72-83. Irinotecan HCl Trihydrate purchased from Selleck.

Purity & Quality Control

Choose Selective Topoisomerase Inhibitors

Biological Activity

Description Irinotecan prevents DNA from unwinding by inhibition of topoisomerase 1.
Features Irinotecan is a prodrug that is used to treat metastatic colorectal cancer.
Targets
Topo I [1]
In vitro

Irinotecan is activated to SN-38 by carboxylesterases to become able to interact with its target, topoisomerase I. Irinotecan induces similar amounts of cleavable complexes at its IC50 in LoVo cells and HT-29 cell lines. SN-38 induces a concentration-dependent formation of cleavable complexes, which is not significantly different in LoVo cells and HT-29 cell lines. Cell accumulation of Irinotecan is markedly different, reaching consistently higher levels in HT-29 cells than in LoVo cells. [1] The lactone E-ring of Irinotecan and SN-38 hydrolyses reversibly in aqueous solutions, and the interconversion between the lactone and carboxylate forms is dependent on pH and temperature. Liver is primarily responsible for the activation of Irinotecan to SN-38. At equal concentrations of Irinotecan and SN-38 glucuronide, the rate of beta-glucuronidase-mediated SN-38 production is higher than that formed from Irinotecan in both tumour and normal tissue. [2] Irinotecan is also converted to SN-38 in intestines, plasma and tumor tissues. [3] Irinotecan is significantly more active in SCLC than in NSCLC cell lines, whereas no significant difference between histological types is observed with SN-38. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
mouse bone marrow cell Mk\SR5l1d3SxeHnjbZR6KGG|c3H5 NYjGXHB{S3m2b4TvfIlkcXS7IHHnZYlve3RibX;1d4Uh[m:wZTDtZZJzd3diY3XscEBjgSCFRmWtS20h[XO|YYmuJGlEPTB;MD6wNFEh|ryP MYeyNVM1OTZ5NB?=
PC3 cells NE\IRXVEgXSxdH;4bYNqfHliYYPzZZk> MlfyO|IhcA>? NGnNb3VEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBRSzNiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JIFt[W2jcjDicJVmKGG|c3H5MkBKSzVyPUCuNFQh|ryP MViyNVM1OTZ5NB?=
A375 cells MXfDfZRwfG:6aXPpeJkh[XO|YYm= MYq3NkBp NGi4UXREgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBCOzd3IHPlcIx{KGGodHXyJFczKGi{czDifUBidGGvYYKgZox2\SCjc4PhfU4hUUN3ME2wMlA1KM7:TR?= MXqyNVM1OTZ5NB?=
LNCAP cells MlPDR5l1d3SxeHnjbZR6KGG|c3H5 M{iwTlczKGh? M{HMXWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGxPS0GSIHPlcIx{KGGodHXyJFczKGi{czDifUBidGGvYYKgZox2\SCjc4PhfU4hUUN3ME2wMlA6KM7:TR?= MUGyNVM1OTZ5NB?=
MESSA cells MoHzR5l1d3SxeHnjbZR6KGG|c3H5 NHHXOmg4OiCq MnL1R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWVUW0FiY3XscJMh[W[2ZYKgO|IhcHK|IHL5JIFt[W2jcjDicJVmKGG|c3H5MkBKSzVyPUCuNFEh|ryP MkDNNlE{PDF4N{S=
H460 cells MUXDfZRwfG:6aXPpeJkh[XO|YYm= MkfuO|IhcA>? MVLDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIOFYxKGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDhcIFu[XJiYnz1[UBie3OjeT6gTWM2OD1yLkCxOUDPxE1? M3nT[|IyOzRzNke0
MES-SA/Dx5 cells Ml[3R5l1d3SxeHnjbZR6KGG|c3H5 NFO1OZI4OiCq M1XxZWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1GWy2VQT;EfFUh[2WubIOgc5ZmemW6cILld5NqdmdiTVTSNUBi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO|YYmuJGlEPTB;MD6wNlIh|ryP MVeyNVM1OTZ5NB?=
H69 cells MYnDfZRwfG:6aXPpeJkh[XO|YYm= M{Xz[|czKGh? M37WcWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGg3QSClZXzsd{Bi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO|YYmuJGlEPTB;MD6wNlIh|ryP NVe5fldjOjF|NEG2O|Q>
IGROV1 cells NYDJNmx5S3m2b4TvfIlkcXS7IHHzd4F6 NFrTRWc4OiCq NHHqTHZEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBKT1KRVkGgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KGGuYX3hdkBjdHWnIHHzd4F6NiCLQ{WwQVAvODNizszN MXeyNVM1OTZ5NB?=
SK-MEL-2 cells M{HBPWN6fG:2b4jpZ4l1gSCjc4PhfS=> MmmyO|IhcA>? NWfEd4U2S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW0tvTVXMMVIh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IHHsZY1ieiCkbIXlJIF{e2G7LjDJR|UxRTBwMTFOwG0> MmXqNlE{PDF4N{S=
MALME-3M cells MV;DfZRwfG:6aXPpeJkh[XO|YYm= NXTiPVB2PzJiaB?= Mk\ZR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWFNVUVvM12gZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KGGuYX3hdkBjdHWnIHHzd4F6NiCLQ{WwQVAvOiEQvF2= NGPKRZYzOTN2MU[3OC=>
DU145 cells M3Xxd2N6fG:2b4jpZ4l1gSCjc4PhfS=> NXjKN45PPzJiaB?= Mnn2R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gSHUyPDViY3XscJMh[W[2ZYKgO|IhcHK|IHL5JIFt[W2jcjDicJVmKGG|c3H5MkBKSzVyPUCuNkDPxE1? M370bVIyOzRzNke0
HT-29 cells NF7xPGFEgXSxdH;4bYNqfHliYYPzZZk> MUS3NkBp MUXDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDIWE0zQSClZXzsd{Bi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO|YYmuJGlEPTB;MD6yNkDPxE1? NYW3NYg1OjF|NEG2O|Q>
H69AR cells MVrDfZRwfG:6aXPpeJkh[XO|YYm= NXTmS|M{PzJiaB?= Mme4R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTFY6SVJiY3XscJMhd3[ncnX4dJJme3OrbnegUWRTOSCjZoTldkA4OiCqcoOgZpkh[WyjbXHyJIJtfWViYYPzZZkvKEmFNUC9NE4zPSEQvF2= Mn\MNlE{PDF4N{S=
MCF7 cells MmHiR5l1d3SxeHnjbZR6KGG|c3H5 M13KdVI1KGh? NIPzV2JEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOS0Z5IHPlcIx{KGG|c3Xzd4VlKGG|IILl[JVkfGmxbjDpckBk\WyuII\pZYJqdGm2eTDh[pRmeiB{NDDodpMh[nliTWTTJIF{e2G7LjDJR|UxRTBwNTFOwG0> M2n0clI3QDRzMU[4
HCT116 NXS0[mNwTnWwY4Tpc44h[XO|YYm= NXXNZllCS2:vcH;1coQhf2G|IITld5Rm\CCrbjD2bZRzdyCob4KgZ5l1d3SxeHnjbZR6KGGpYXnud5QhUEOWMUG2MEBpfW2jbjDjc4xwdiClYX7j[ZIh[2WubIOgLJRigG:uLYLld4l{fGGwdDmgZZQh[SCmcoXnJINwdmOnboTyZZRqd25icILv[JVkcW6pIEWwKUBqdmirYnn0bY9vKG:oIHPvcI9vgSCob4LtZZRqd25wIFnDOVA:OC53NDFOwG0> MVixNVk3PTN4Mh?=
RPMI8402 MYjDfZRwfG:6aXPpeJkh[XO|YYm= MVO0JIRigXN? M2jzRWN6fG:2b4jpZ{Bi[3Srdnn0fUBi\2GrboP0JIh2dWGwIHz5cZBpd2KuYYP0JJR2dW:{IHPlcIwhdGmwZTDSVG1KQDRyMjDh[pRmeiB2IHThfZMhd2ZidILlZZRu\W62LjDJR|UxRTBwNUeg{txO Mn\zNVI4PDd5OUi=
KB3-1 cells MnW3R5l1d3SxeHnjbZR6KGG|c3H5 NYrHXHRxS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hU0J|LUGgZ4VtdHNiYomgUXRVKG2ndHjv[E4hUUN3ME2wMlY5KM7:TR?= MVOxPFc4OTl|MB?=
PC3 cells NV6zV2l6WHKxbHnm[ZJifGmxbjDhd5NigQ>? NHn0SpA4OiCq M{DzTmFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iUFOzJINmdGy|IHHzd4V{e2WmIHHzJINmdGy3bHHyJGRPSSClb370[Y51KGGodHXyJFczKGi{czDifUBEgVGXQV7UJG5HKG[udX;y[ZNk\W6lZTDhd5NigS5iSVO1NF0xNjhizszN M37LfFI3PzNzM{Cw
A549 cells MlP4R5l1d3SxeHnjbZR6KGG|c3H5 NHu0UoQzPCCq MYjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJIF{e2W|c3XkJIF{KHKnZIXjeIlwdiCrbjDj[YxtKH[rYXLpcIl1gSCjZoTldkAzPCCqcoOgZpkhVVSVIHHzd4F6NiCLQ{WwQVAvQCEQvF2= NHLlVmszPjh2MUG2PC=>
MCF7 cells M3fnPHBzd2yrZnXyZZRqd25iYYPzZZk> MnjiPVYhcA>? MY\BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKE2FRkegZ4VtdHNiYYPz[ZN{\WRiYYOgZ4VtdHWuYYKgSG5CKGOxboTlcpQh[W[2ZYKgPVYhcHK|IHL5JGN6WVWDTmSgUmYh\my3b4Lld4NmdmOnIHHzd4F6NiCLQ{WwQVAvQSEQvF2= NV31eGI2OjZ5M{GzNFA>
HepG2 cells NHjPUpVEgXSxdH;4bYNqfHliYYPzZZk> NGPCO3AzPCCq NXXR[Wc4S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUGWyR{KgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJIlvKGOnbHygeoli[mmuaYT5JIFnfGW{IEK0JIhzeyCkeTDNWHMh[XO|YYmuJGlEPTB;MD65JO69VQ>? NGnVOGozPjh2MUG2PC=>
MDA-MB-435 cells MkHLR5l1d3SxeHnjbZR6KGG|c3H5 NUm1Z2ZlPzJiaB?= M3nObWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1FSS2PQj20N|Uh[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IF3UWEBie3OjeT6gTWM2OD1zLkG0JO69VQ>? NGPCc4kzODN5MUG4Ny=>
LS174T cells M3\3dmN6fG:2b4jpZ4l1gSCjc4PhfS=> MWG5OkBp M1fy[WN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGxUOTd2VDDj[YxteyCjZoTldkA6PiCqcoOgZpkhVVSWIHHzd4F6NiCLQ{WwQVEvOTZizszN M4HNNVE5PTF|OUe2
T84 cells NXLRdXhsWHKxbHnm[ZJifGmxbjDhd5NigQ>? NV34W|BTQTZiaB?= MWTBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFR6NDDj[YxteyCjc4Pld5Nm\CCjczDj[YxtfWyjcjDEUmEh[2:wdHXueEBi\nSncjC5OkBpenNiYomgR5lSXUGQVDDOSkBndHWxcnXzZ4Vv[2ViYYPzZZkvKEmFNUC9NU4zKM7:TR?= M4fDWVI3PzNzM{Cw
SW480 cells M{DJVmN6fG:2b4jpZ4l1gSCjc4PhfS=> M2Lyb|I1KGh? NYLrXnhjS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1d2OECgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJIlvKGOnbHygeoli[mmuaYT5JIFnfGW{IEK0JIhzeyCkeTDNWHMh[XO|YYmuJGlEPTB;MT60JO69VQ>? M13KcVI3QDRzMU[4
K562 cells NVTWXlZkWHKxbHnm[ZJifGmxbjDhd5NigQ>? M1\pVlczKGh? NXLqWHp4SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDLOVYzKGOnbHzzJIFnfGW{IEeyJIhzey5iSVO1NF0yNjlizszN NYHKfodWOjV2MkCxO|U>
HT-29 cells M2HITXBzd2yrZnXyZZRqd25iYYPzZZk> Mn30O|IhcA>? MVPBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiWLUK5JINmdGy|IHHzd4V{e2WmIHHzJINmdGy3bHHyJGRPSSClb370[Y51KGGodHXyJFczKGi{czDifUBEgVGXQV7UJG5HKG[udX;y[ZNk\W6lZTDhd5NigS5iSVO1NF0yNjlizszN MkjpNlY4OzF|MEC=
HCT116 cells NYP2R202WHKxbHnm[ZJifGmxbjDhd5NigQ>? MlLUNlQuPzJiaB?= NF70bZpCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFjDWFEyPiClZXzsd{Bi\nSncjCyOEB1dyB5MjDodpMh[nliU2LCJIF{e2G7LjDJR|UxRTJizszN MVuyOlU6PTh5NR?=
Hep3B cells MmK1VJJwdGmoZYLheIlwdiCjc4PhfS=> NFHIOXc4OiCq Mk\iRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKZYCzRkBk\WyuczDh[pRmeiB5MjDodpMh[nliWGTUJIF{e2G7LjDJR|UxRTRwN{Og{txO M{P6UVE6Pzl4OUW2
Hep3B cells M333Rmdzd3e2aDDpcohq[mm2b36gZZN{[Xl? NHHtTY84OiCq M4HMNWdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJGhmeDOEIHPlcIx{KGGodHXyJFczKGi{czDifUBZXFRiYYPzZZkvKEmFNUC9OE44OyEQvF2= NHG3WZUzOjB5OUK1OC=>
LoVo cells NWriSVFmS3m2b4TvfIlkcXS7IHHzd4F6 NUnz[|VJPzJiaB?= MnrIR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUI9XdyClZXzsd{Bi\nSncjC3NkBpenNiYomgUXRVKGG|c3H5MkBKSzVyPUSuPVkh|ryP NYmxVYZTOjB|N{GxPFM>
KBH5.0 cells M3i3eWN6fG:2b4jpZ4l1gSCjc4PhfS=> M3TKbWN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGtDUDVwMDDj[YxteyCkeTDNWHQhdWW2aH;kMkBKSzVyPUeuOEDPxE1? NWTEVZBiOTh5N{G5N|A>
H3347 cells NU\PWphuS3m2b4TvfIlkcXS7IHHzd4F6 NX;wSZI2PzJiaB?= NXzmeZgyS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUDN|NEegZ4VtdHNiYYPz[ZN{\WRiYYOg[5Jwf3SqIHnubIljcXSrb36gZYZ1\XJiN{KgbJJ{KGK7IFHsZY1ieiCEbIXlJIF{e2G7LjDJR|UxRTdwNUOg{txO MUCyOFU5OzN3NR?=
HCT15 cells MmXvVJJwdGmoZYLheIlwdiCjc4PhfS=> Mm\INlQuPzJiaB?= MknVRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6|dDDoeY1idiCKQ2SxOUBk\WyuczDh[pRmeiB{NDD0c{A4OiCqcoOgZpkhW1KEIHHzd4F6NiCLQ{WwQVgvPSEQvF2= NF[zU|MzPjV7NUi3OS=>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
AMPK / p-AMPK / mTOR / p-mTOR / p70S6K / p-p70S6K; 

PubMed: 25973791     


Western blot showing the protein levels of AMPK, p-AMPK, mTOR, p-mTOR, p70S6K, and p-p70S6K in LoVo and LoVo-R8 with or without irinotecan. 

NFκB p65 / phospho-NFκB p65 / NFκB p50 / IκBα / p27Kip1; 

PubMed: 22206574     


For Western blot analysis (B), cytoplasmic proteins were analyzed using antibodies against NFκB p65 and p50, phospho-NFκB p65, IκBα and p27Kip1. In the presence of irinotecan, there was a loss of cytoplasmic NF-κBp65, but in the presence of sorafenib, this loss was greatly reduced, corresponding to a decrease in phosphorylation of NF-κBp65. In addition, compared to treatment with sorafenib or irinotecan alone, there was increased expression of IκBα following treatment with sorafenib and irinotecan. Lastly, following treatment with irinotecan and sorafenib irinotecan combination, there was decreased expression of p27Kip1 compared to sorafenib treatment alone.

TopI / pAKT / pMEK / pERK / p-p38 MAPK / pJNK2; 

PubMed: 29237470     


a Gimatecan significantly inhibited the expression of TopI, pAKT, pMEK, and pERK, and activated the expression of p-p38 MAPK and pJNK2 in SNU-1 cells. b Gimatecan significantly inhibited the expression of pAKT and pERK in NCI-N87 cells. Cells were starved in serum-free medium overnight, exposed to gimatecan or irinotecan for 48 h and harvested at 70–80% confluence. Total protein of SNU-1 and NCI-N87 was extracted and the expression of TopI, pAKT, pMEK, pERK, p-p38 MAPK and pJNK2 were assessed by western-blotting 

25973791 22206574 29237470
Immunofluorescence
NFκB; 

PubMed: 22206574     


BT12 cells were incubated with sorafenib or vehicle for 30 minutes followed by treatment with irinotecan for an additional 2 hours. For indirect immunofluorescence (A), cells were fixed and stained with antibodies to NF-κB followed by fluorescent labeled secondary antibodies. Concurrent DAPI stain was used to localize the nuclei (lower panel). Slides were visualized using a fluorescent microscope and random fields were photographed. The cytoplasmic staining seen in untreated and sorafenib treated cells was significantly reduced following treatment with irinotecan. However, the addition of sorafenib enabled the cells to maintain cytoplasmic staining in the presence of irinotecan. 

22206574
Growth inhibition assay
Cell viability; 

PubMed: 25973791     


The sensitivity of eight colon cancer cell lines to irinotecan was measured using the CCK-8 assay. For the CCK-8 assay, cells were exposed to irinotecan at given concentrations for 72 h before measurement. The cell viability was presented as the percentage relative to untreated cells.

25973791
In vivo In COLO 320 xenografts, Irinotecan induces a maximum growth inhibition of 92%. [5] A single dose of Irinotecan significantly increases amounts of topoisomerase I covalently bound to DNA in stomach, duodenum, colon and liver. Concomitantly, the Irinotecan-treated group shows significantly higher amounts of DNA strand breaks in colon mucosa cells compared to the control group. [6]

Protocol

Cell Research:

[1]

+ Expand
  • Cell lines: LoVo and HT-29 cells
  • Concentrations: 0 μM -100 μM
  • Incubation Time: 48 hours
  • Method:

    Exponentially growing cells (LoVo and HT-29 cells) are seeded in 20 cm2 Petri dishes with an optimal cell number for each cell line (2 × 104 for LoVo cells, 105 for HT-29 cells). They are treated 2 days later with increasing concentrations of Irinotecan or SN-38 for one cell doubling time (24 hours for LoVo cells, 40 hours for HT-29 cells). After washing with 0.15 M NaCl, the cells are further grown for two doubling times in normal medium, detached from the support with trypsin-EDTA and counted in a hemocytometer. The IC50 values are then estimated as the Irinotecan or SN-38 concentrations responsible for 50% growth inhibition as compared with cells incubated without Irinotecan or SN-38.


    (Only for Reference)
Animal Research:

[5]

+ Expand
  • Animal Models: Female nude mice with COLO 320 and WiDr xenografts.
  • Formulation: 0.9% NaCl
  • Dosages: 20 mg/kg
  • Administration: Intraperitoneal injection
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 100 mg/mL (147.67 mM)
Ethanol 7 mg/mL (10.33 mM)
Water 1 mg/mL (1.47 mM)
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+saline
For best results, use promptly after mixing.
20mg/mL

* 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.

Chemical Information

Molecular Weight 677.18
Formula

C33H38N4O6.HCl.3H2O

CAS No. 136572-09-3
Storage powder
in solvent
Synonyms CPT-11 HCl Trihydrate

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    Volume
    Molecular Weight

*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).

Dilution Calculator

Dilution Calculator

Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:

Concentration (start) x Volume (start) = Concentration (final) x Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )

  • C1
    V1
    C2
    V2

* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).

The Serial Dilution Calculator Equation

  • Serial Dilutions

  • Computed Result

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
Molecular Weight Calculator

Molecular Weight Calculator

Enter the chemical formula of a compound to calculate its molar mass and elemental composition:

Total Molecular Weight: g/mol

Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2

Instructions to calculate molar mass (molecular weight) of a chemical compound:

To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.

Definitions of molecular mass, molecular weight, molar mass and molar weight:

Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.

Molarity Calculator

Mass Concentration Volume Molecular Weight

Clinical Trial Information

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT03641313 Not yet recruiting Clinical Stage III Gastric Cancer AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IV Gastric Cancer AJCC v8|Clinical Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVA Gastric Cancer AJCC v8|Clinical Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVB Gastric Cancer AJCC v8|Clinical Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Metastatic Gastric Adenocarcinoma|Metastatic Gastroesophageal Junction Adenocarcinoma|Pathologic Stage III Gastric Cancer AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastric Cancer AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastric Cancer AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIC Gastric Cancer AJCC v8|Pathologic Stage IV Gastric Cancer AJCC v8|Pathologic Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage III Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IV Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|TP53 Gene Mutation|Unresectable Gastroesophageal Junction Adenocarcinoma National Cancer Institute (NCI) July 1 2019 Phase 2
NCT03641313 Not yet recruiting Clinical Stage III Gastric Cancer AJCC v8|Clinical Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IV Gastric Cancer AJCC v8|Clinical Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVA Gastric Cancer AJCC v8|Clinical Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Clinical Stage IVB Gastric Cancer AJCC v8|Clinical Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Metastatic Gastric Adenocarcinoma|Metastatic Gastroesophageal Junction Adenocarcinoma|Pathologic Stage III Gastric Cancer AJCC v8|Pathologic Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIA Gastric Cancer AJCC v8|Pathologic Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIB Gastric Cancer AJCC v8|Pathologic Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IIIC Gastric Cancer AJCC v8|Pathologic Stage IV Gastric Cancer AJCC v8|Pathologic Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Pathologic Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage III Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage III Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IIIB Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IV Gastric Cancer AJCC v8|Postneoadjuvant Therapy Stage IV Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVA Gastroesophageal Junction Adenocarcinoma AJCC v8|Postneoadjuvant Therapy Stage IVB Gastroesophageal Junction Adenocarcinoma AJCC v8|TP53 Gene Mutation|Unresectable Gastroesophageal Junction Adenocarcinoma National Cancer Institute (NCI) July 1 2019 Phase 2
NCT03861702 Not yet recruiting Locally Advanced Pancreatic Carcinoma(LAPC) Big Ten Cancer Research Consortium|Ipsen June 2019 Phase 2
NCT03883919 Not yet recruiting Pancreatic Cancer|Pancreas Cancer|Cancer of the Pancreas Washington University School of Medicine|Ipsen June 30 2019 Phase 1
NCT03861702 Not yet recruiting Locally Advanced Pancreatic Carcinoma(LAPC) Big Ten Cancer Research Consortium|Ipsen June 2019 Phase 2
NCT03883919 Not yet recruiting Pancreatic Cancer|Pancreas Cancer|Cancer of the Pancreas Washington University School of Medicine|Ipsen June 30 2019 Phase 1

Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

Tel: +1-832-582-8158 Ext:3

If you have any other enquiries, please leave a message.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID