Irinotecan HCl Trihydrate

Catalog No.S2217 Synonyms: CPT-11 HCl Trihydrate

Molecular Weight(MW): 677.18

Irinotecan prevents DNA from unwinding by inhibition of topoisomerase 1.

Cited by 10 Publications

Neoplasia, 2019, 21(1):146-155

PubMed: 30562637 ( click the link to review the publication )

Theranostics, 2018, 8(5):1312-1326

PubMed: 29507622 ( click the link to review the publication )

Mol Cancer Ther, 2018, 17(12):2551-2563

PubMed: 30217967 ( click the link to review the publication )

Mol Cancer Ther, 2018, 17(2):508-520

PubMed: 29167313 ( click the link to review the publication )

Carcinogenesis, 2018, 39(1):72-83

PubMed: 29106445 ( click the link to review the publication )

Mol Carcinog, 2018, 57(10):1383-1395

PubMed: 29917295 ( click the link to review the publication )

Cancer Biol Ther, 2018, 19(9):835-846

PubMed: 30067423 ( click the link to review the publication )

J Am Soc Mass Spectrom, 2018, 29(3):516-526

PubMed: 29209911 ( click the link to review the publication )

Cancer Lett, 2017, 411:35-43

PubMed: 28964784 ( click the link to review the publication )

Biomaterials, 2015, 72:74-89

PubMed: 26344365 ( click the link to review the publication )

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	Incubation Time	Activity Description	PMID
mouse bone marrow cell	NGfISnREgXSxdH;4bYNqfHliYYPzZZk>		MlzvR5l1d3SxeHnjbZR6KGGpYXnud5QhdW:3c3WgZo9v\SCvYYLyc5ch[2WubDDifUBETlVvR12gZZN{[XlwIFnDOVA:OC5yMEGg{txO	MnPwNlE{PDF4N{S=
PC3 cells	M1fMUmN6fG:2b4jpZ4l1gSCjc4PhfS=>	Mkm4O\|IhcA>?	Mkm0R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gVGM{KGOnbHzzJIFnfGW{IEeyJIhzeyCkeTDhcIFu[XJiYnz1[UBie3OjeT6gTWM2OD1yLkC0JO69VQ>?	NWTBV4Z3OjF\|NEG2O\|Q>
A375 cells	NEfRbXJEgXSxdH;4bYNqfHliYYPzZZk>	NFrZdHA4OiCq	NEPocItEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBCOzd3IHPlcIx{KGGodHXyJFczKGi{czDifUBidGGvYYKgZox2\SCjc4PhfU4hUUN3ME2wMlA1KM7:TR?=	MVqyNVM1OTZ5NB?=
LNCAP cells	Mnj4R5l1d3SxeHnjbZR6KGG\|c3H5	M4O1VVczKGh?	Ml:0R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUG5ESVBiY3XscJMh[W[2ZYKgO\|IhcHK\|IHL5JIFt[W2jcjDicJVmKGG\|c3H5MkBKSzVyPUCuNFkh\|ryP	NGDiPWszOTN2MU[3OC=>
MESSA cells	MnPHR5l1d3SxeHnjbZR6KGG\|c3H5	MW[3NkBp	MWrDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDNSXNUSSClZXzsd{Bi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO\|YYmuJGlEPTB;MD6wNUDPxE1?	NF;JOYczOTN2MU[3OC=>
H460 cells	MXTDfZRwfG:6aXPpeJkh[XO\|YYm=	NYLsfIZbPzJiaB?=	NVPyRmh[S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUDR4MDDj[YxteyCjZoTldkA4OiCqcoOgZpkh[WyjbXHyJIJtfWViYYPzZZkvKEmFNUC9NE4xOTVizszN	M{Xr[lIyOzRzNke0
MES-SA/Dx5 cells	NHi2NYFEgXSxdH;4bYNqfHliYYPzZZk>	NWLwO201PzJiaB?=	M1;wWmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJG1GWy2VQT;EfFUh[2WubIOgc5ZmemW6cILld5NqdmdiTVTSNUBi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO\|YYmuJGlEPTB;MD6wNlIh\|ryP	NHPmcHQzOTN2MU[3OC=>
H69 cells	NFrsb2NEgXSxdH;4bYNqfHliYYPzZZk>	NXzTRnNSPzJiaB?=	M37GfmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGg3QSClZXzsd{Bi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO\|YYmuJGlEPTB;MD6wNlIh\|ryP	NXLXTm9GOjF\|NEG2O\|Q>
IGROV1 cells	NHTDTXlEgXSxdH;4bYNqfHliYYPzZZk>	MV23NkBp	NVXJeJVPS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUUeUT2[xJINmdGy\|IHHmeIVzKDd{IHjyd{BjgSCjbHHtZZIh[my3ZTDhd5NigS5iSVO1NF0xNjB\|IN88US=>	NH\iS\|kzOTN2MU[3OC=>
SK-MEL-2 cells	MmDlR5l1d3SxeHnjbZR6KGG\|c3H5	NVXlXWg1PzJiaB?=	M2ThT2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJHNMNU2HTD2yJINmdGy\|IHHmeIVzKDd{IHjyd{BjgSCjbHHtZZIh[my3ZTDhd5NigS5iSVO1NF0xNjFizszN	MmP5NlE{PDF4N{S=
MALME-3M cells	MX;DfZRwfG:6aXPpeJkh[XO\|YYm=	MUi3NkBp	NX;kVJV6S3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hVUGOTVWtN20h[2WubIOgZYZ1\XJiN{KgbJJ{KGK7IHHsZY1ieiCkbIXlJIF{e2G7LjDJR\|UxRTBwMjFOwG0>	MYeyNVM1OTZ5NB?=
DU145 cells	NVjTcFNKS3m2b4TvfIlkcXS7IHHzd4F6	NXXCZZBqPzJiaB?=	MXLDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDEWVE1PSClZXzsd{Bi\nSncjC3NkBpenNiYomgZYxidWG{IHLseYUh[XO\|YYmuJGlEPTB;MD6yJO69VQ>?	M1TEVVIyOzRzNke0
HT-29 cells	NXqwTWpMS3m2b4TvfIlkcXS7IHHzd4F6	MmO4O\|IhcA>?	NWfrPGFGS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUFRvMkmgZ4VtdHNiYX\0[ZIhPzJiaILzJIJ6KGGuYX3hdkBjdHWnIHHzd4F6NiCLQ{WwQVAvOjJizszN	MV6yNVM1OTZ5NB?=
H69AR cells	M4L5VWN6fG:2b4jpZ4l1gSCjc4PhfS=>	NV;yNpF4PzJiaB?=	NXvMWWltS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hUDZ7QWKgZ4VtdHNib4\ldoV5eHKnc4PpcochVUSUMTDh[pRmeiB5MjDodpMh[nliYXzhcYFzKGKudXWgZZN{[XlwIFnDOVA:OC5{NTFOwG0>	MUCyNVM1OTZ5NB?=
MCF7 cells	MYXDfZRwfG:6aXPpeJkh[XO\|YYm=	M2\qfFI1KGh?	NGfkc\|lEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBOS0Z5IHPlcIx{KGG\|c3Xzd4VlKGG\|IILl[JVkfGmxbjDpckBk\WyuII\pZYJqdGm2eTDh[pRmeiB{NDDodpMh[nliTWTTJIF{e2G7LjDJR\|UxRTBwNTFOwG0>	NEHwXpEzPjh2MUG2PC=>
HCT116	NUTtbnF3TnWwY4Tpc44h[XO\|YYm=		MY\Dc41xd3WwZDD3ZZMhfGW\|dHXkJIlvKH[rdILvJIZweiCleYTveI95cWOrdImgZYdicW6\|dDDIR3QyOTZuIHj1cYFvKGOxbH;uJINidmOncjDj[YxteyBqdHH4c4wuemW\|aYP0ZY51MSCjdDDhJIRzfWdiY3;uZ4VvfHKjdHnvckBxem:mdXPpcochPTBnIHnubIljcXSrb36gc4Yh[2:ub375JIZwem2jdHnvck4hUUN3ME2wMlU1KM7:TR?=	NXHHOHAyOTF7NkWzOlI>
RPMI8402	M4nXN2N6fG:2b4jpZ4l1gSCjc4PhfS=>	M4rPT\|Qh\GG7cx?=	MUXDfZRwfG:6aXOgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCueX3wbI9jdGG\|dDD0eY1weiClZXzsJIxqdmViUmDNTVg1ODJiYX\0[ZIhPCCmYYnzJI9nKHS{ZXH0cYVvfC5iSVO1NF0xNjV5IN88US=>	NHvtd5kyOjd2N{e5PC=>
KB3-1 cells	Mor4R5l1d3SxeHnjbZR6KGG\|c3H5		NWTRc\|RSS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hU0J\|LUGgZ4VtdHNiYomgUXRVKG2ndHjv[E4hUUN3ME2wMlY5KM7:TR?=	MWWxPFc4OTl\|MB?=
PC3 cells	NHLwZ\|dRem:uaX\ldoF1cW:wIHHzd4F6	NYr3PHl4PzJiaB?=	M3TQbWFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iUFOzJINmdGy\|IHHzd4V{e2WmIHHzJINmdGy3bHHyJGRPSSClb370[Y51KGGodHXyJFczKGi{czDifUBEgVGXQV7UJG5HKG[udX;y[ZNk\W6lZTDhd5NigS5iSVO1NF0xNjhizszN	NFfaWZczPjd\|MUOwNC=>
A549 cells	NVPOXmhjS3m2b4TvfIlkcXS7IHHzd4F6	M4LLelI1KGh?	MUjDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDBOVQ6KGOnbHzzJIF{e2W\|c3XkJIF{KHKnZIXjeIlwdiCrbjDj[YxtKH[rYXLpcIl1gSCjZoTldkAzPCCqcoOgZpkhVVSVIHHzd4F6NiCLQ{WwQVAvQCEQvF2=	NWHwS3M2OjZ6NEGxOlg>
MCF7 cells	NIqyc4JRem:uaX\ldoF1cW:wIHHzd4F6	M1\HRlk3KGh?	NX\YT2JFSW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDNR2Y4KGOnbHzzJIF{e2W\|c3XkJIF{KGOnbHz1cIFzKESQQTDjc451\W62IHHmeIVzKDl4IHjyd{BjgSCFeWHVRW5VKE6IIH\seY9z\XOlZX7j[UBie3OjeT6gTWM2OD1yLkmg{txO	MUeyOlc{OTNyMB?=
HepG2 cells	Mn\6R5l1d3SxeHnjbZR6KGG\|c3H5	NFu4dGUzPCCq	MkL6R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gTIVxTzJiY3XscJMh[XO\|ZYPz[YQh[XNicnXkeYN1cW:wIHnuJINmdGxidnnhZoltcXS7IHHmeIVzKDJ2IHjyd{BjgSCPVGOgZZN{[XlwIFnDOVA:OC57IN88US=>	M4POU\|I3QDRzMU[4
MDA-MB-435 cells	MofQR5l1d3SxeHnjbZR6KGG\|c3H5	MofiO\|IhcA>?	MnzSR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gUWRCNU2ELUSzOUBk\WyuczDh[pRmeiB5MjDodpMh[nliTWTUJIF{e2G7LjDJR\|UxRTFwMUSg{txO	MXiyNFM4OTF6Mx?=
LS174T cells	NEHUXIZEgXSxdH;4bYNqfHliYYPzZZk>	NVrQS4JUQTZiaB?=	M{nNXGN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGxUOTd2VDDj[YxteyCjZoTldkA6PiCqcoOgZpkhVVSWIHHzd4F6NiCLQ{WwQVEvOTZizszN	MUOxPFUyOzl5Nh?=
T84 cells	M1jVWnBzd2yrZnXyZZRqd25iYYPzZZk>	NITsRZc6PiCq	MV;BcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKFR6NDDj[YxteyCjc4Pld5Nm\CCjczDj[YxtfWyjcjDEUmEh[2:wdHXueEBi\nSncjC5OkBpenNiYomgR5lSXUGQVDDOSkBndHWxcnXzZ4Vv[2ViYYPzZZkvKEmFNUC9NU4zKM7:TR?=	MoPMNlY4OzF\|MEC=
SW480 cells	NV;KVoo{S3m2b4TvfIlkcXS7IHHzd4F6	NEjrVIszPCCq	NUTBWWhFS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hW1d2OECgZ4VtdHNiYYPz[ZN{\WRiYYOgdoVlfWO2aX;uJIlvKGOnbHygeoli[mmuaYT5JIFnfGW{IEK0JIhzeyCkeTDNWHMh[XO\|YYmuJGlEPTB;MT60JO69VQ>?	M13BNVI3QDRzMU[4
K562 cells	MX;Qdo9tcW[ncnH0bY9vKGG\|c3H5	M{njclczKGh?	NFTuNnlCdnSrcILvcIln\XKjdHn2[UBi[3Srdnn0fUBi\2GrboP0JIh2dWGwIFu1OlIh[2WubIOgZYZ1\XJiN{KgbJJ{NiCLQ{WwQVEvQSEQvF2=	M1LjOVI2PDJyMUe1
HT-29 cells	NFWyWZdRem:uaX\ldoF1cW:wIHHzd4F6	MmPTO\|IhcA>?	M1;0WGFvfGmycn;sbYZmemG2aY\lJIFkfGm4aYT5JIFo[Wmwc4SgbJVu[W5iSGStNlkh[2WubIOgZZN{\XO\|ZXSgZZMh[2WubIXsZZIhTE6DIHPvcpRmdnRiYX\0[ZIhPzJiaILzJIJ6KEO7UWXBUnQhVkZiZnz1c5Jme2OnbnPlJIF{e2G7LjDJR\|UxRTFwOTFOwG0>	MYKyOlc{OTNyMB?=
HCT116 cells	NWrjeXViWHKxbHnm[ZJifGmxbjDhd5NigQ>?	NYHmZpJEOjRvN{KgbC=>	MoPJRY51cXC{b3zp[oVz[XSrdnWgZYN1cX[rdImgZYdicW6\|dDDoeY1idiCKQ2SxNVYh[2WubIOgZYZ1\XJiMkSgeI8hPzJiaILzJIJ6KFOUQjDhd5NigS5iSVO1NF0zKM7:TR?=	MViyOlU6PTh5NR?=
Hep3B cells	MlXuVJJwdGmoZYLheIlwdiCjc4PhfS=>	NYn4[XR4PzJiaB?=	NWDHXJI4SW62aYDyc4xq\mW{YYTpeoUh[WO2aY\peJkh[WejaX7zeEBpfW2jbjDI[ZA{SiClZXzsd{Bi\nSncjC3NkBpenNiYomgXHRVKGG\|c3H5MkBKSzVyPUSuO\|Mh\|ryP	MY[xPVc6Pjl3Nh?=
Hep3B cells	MVTHdo94fGhiaX7obYJqfG:wIHHzd4F6	NXTUUXZ2PzJiaB?=	M2jOTmdzd3e2aDDpcohq[mm2aX;uJI9nKGi3bXHuJGhmeDOEIHPlcIx{KGGodHXyJFczKGi{czDifUBZXFRiYYPzZZkvKEmFNUC9OE44OyEQvF2=	MlzrNlIxPzl{NUS=
LoVo cells	NWDZ[2psS3m2b4TvfIlkcXS7IHHzd4F6	MYW3NkBp	M1PFS2N6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGxwXm9iY3XscJMh[W[2ZYKgO\|IhcHK\|IHL5JG1VXCCjc4PhfU4hUUN3ME20Mlk6KM7:TR?=	NH23e2IzODN5MUG4Ny=>
KBH5.0 cells	NHLqemJEgXSxdH;4bYNqfHliYYPzZZk>		NE\DTJVEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBMSkh3LkCgZ4VtdHNiYomgUXRVKG2ndHjv[E4hUUN3ME23MlQh\|ryP	MlLONVg4PzF7M{C=
H3347 cells	MX7DfZRwfG:6aXPpeJkh[XO\|YYm=	NInCUVA4OiCq	NGnOdGdEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBJOzN2NzDj[YxteyCjc4Pld5Nm\CCjczDndo94fGhiaX7obYJqfGmxbjDh[pRmeiB5MjDodpMh[nliQXzhcYFzKEKudXWgZZN{[XlwIFnDOVA:Py53MzFOwG0>	MWGyOFU5OzN3NR?=
HCT15 cells	NY\MR2tCWHKxbHnm[ZJifGmxbjDhd5NigQ>?	NITDXIEzPC15MjDo	MWTBcpRqeHKxbHnm[ZJifGm4ZTDhZ5Rqfmm2eTDh[4FqdnO2IHj1cYFvKEiFVEG1JINmdGy\|IHHmeIVzKDJ2IITvJFczKGi{czDifUBUWkJiYYPzZZkvKEmFNUC9PE42KM7:TR?=	NFrydFMzPjV7NUi3OS=>

... 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 PLoS One 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 Cancer Cell Int 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 J Transl Med 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 Cancer Cell Int 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 PLoS One 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)

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)

References

+ Expand

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 Download Irinotecan HCl Trihydrate SDF

Molecular Weight	677.18
Formula	C₃₃H₃₈N₄O₆.HCl.3H₂O
CAS No.	136572-09-3
Storage	3 years -20°C powder
Storage	2 years -80°C in solvent
Synonyms	CPT-11 HCl Trihydrate

Bio Calculators

Molarity Calculator

Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

*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

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 )

* 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
Concertration (start):
Dilution-folds:

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

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

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

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

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.

Topoisomerase Signaling Pathway Map

Related Topoisomerase Products0

SCR7 ^New

SCR7 is a specific DNA Ligase IV inhibitor, which blocks nonhomologous end-joining (NHEJ). It increases the efficiency of HDR-mediated genome editing up to 19-fold using CRISPR/Cas9 in mammalian cells and mouse embryos.
Blasticidin S HCl ^New

Blasticidin S HCl is a nucleoside antibiotic isolated from Stretomyces girseochromogenes, and acts as a DNA and protein synthesis inhibitor, used to select transfected cells carrying bsr or BSD resistance genes.
LMK-235 ^New

LMK-235 is a selective inhibitor of HDAC4 and HDAC5 with IC50 of 11.9 nM and 4.2 nM, respectively.
Doxorubicin (Adriamycin) HCl

Doxorubicin (Adriamycin) HCl is an antibiotic agent that inhibits DNA topoisomerase II and induces DNA damage and apoptosis in tumor cells.
Etoposide

Etoposide is a semisynthetic derivative of podophyllotoxin, which inhibits DNA synthesis via topoisomerase II inhibition activity.
Camptothecin

Camptothecin is a specific inhibitor of DNA topoisomerase I (Topo I) with IC50 of 0.68 μM in a cell-free assay. Phase 2.
Daunorubicin HCl

Daunorubicin HCl inhibits both DNA and RNA synthesis and inhibits DNA synthesis with K_i of 0.02 μM in a cell-free assay.
SN-38

SN-38 is an active metabolite of CPT-11, inhibits DNA topoisomerase I, DNA synthesis and causes frequent DNA single-strand breaks.
Topotecan HCl

Topotecan HCl is a topoisomerase I inhibitor for MCF-7 Luc cells and DU-145 Luc cells with IC50 of 13 nM and 2 nM in cell-free assays, respectively.

Features:Topotecan is a water-soluble derivative of camptothecin.
Idarubicin HCl

Idarubicin HCl is a hydrochloride salt form of Idarubicin which is an anthracycline antibiotic and a DNA topoisomerase II (topo II) inhibitor for MCF-7 cells with IC50 of 3.3 ng/mL in a cell-free assay.

Features:Idarubicin is a substrate for CYP450 2D6 and 2C9.

Choose Your Country or Region

By Signaling Pathways

By product type

Irinotecan HCl Trihydrate

Cited by 10 Publications

4 Customer Reviews

Purity & Quality Control

Choose Selective Topoisomerase Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Irinotecan HCl Trihydrate SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

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

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

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

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

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

Tech Support

Topoisomerase Signaling Pathway Map

Related Topoisomerase Products0

Choose Your Country or Region

By Signaling Pathways

By product type

Irinotecan HCl Trihydrate

Cited by 10 Publications

4 Customer Reviews

Purity & Quality Control

Choose Selective Topoisomerase Inhibitors

Biological Activity

Protocol

References

Solubility (25°C)

Chemical Information Download Irinotecan HCl Trihydrate SDF

Bio Calculators

Molarity Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Dilution Calculator

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

The Serial Dilution Calculator Equation

Serial Dilutions

Computed Result

Molecular Weight Calculator

Total Molecular Weight: g/mol

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

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

Molarity Calculator

Clinical Trial Information (data from https://clinicaltrials.gov, updated on 2019-03-27)

Tech Support

Topoisomerase Signaling Pathway Map

Related Topoisomerase Products0

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