PD184352 (CI-1040)

Catalog No.S1020

PD184352 (CI-1040) Chemical Structure

Molecular Weight(MW): 478.67

PD184352 (CI-1040) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM in cell-based assays, 100-fold more selective for MEK1/2 than MEK5. Phase 2.

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Cited by 45 Publications

13 Customer Reviews

  • The inhibitor PD173074 (A) or PD184352 (B) was administered to one uterine horn of Hand2d/d mice on day 3 of pregnancy (n = 5). The other horn served as vehicle-treated control. Uterine horns were collected on the morning of day 4, and sections were subjected to IHC to detect p-FRS2, p-ERK1/2, and Ki-67. (C) IHC of pERa and Muc-1 in uterine sections of Hand2d/d mice treated with PD173074 or PD184352.

    Science 2011 331, 912-916. PD184352 (CI-1040) purchased from Selleck.

     

    Melanoma cell viability and in vivo growth by cyclindependent kinase 2/4 inhibition. Western blot analysis for c-Jun, phosphorylated-ERK1/2 (Thr202/Tyr204) (p-ERK1/2), and total ERK1/2 protein levels was done for human melanoma cell lines treated with the BRAFV600E inhibitor GDC-0879 (1 μM), or MEK inhibitors CI-1040 (1 μM), U0126 (1 μM), and PD98059 (10 μM) for 18 hours.

    J Natl Cancer Inst 2012 104(21), 1673-9. PD184352 (CI-1040) purchased from Selleck.

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    Melanoma cell viability and in vivo growth by cyclindependent kinase 2/4 inhibition. In vivo growth of LOXIMVI xenografts in athymic nude Foxn1nu mice is shown. Tumors were allowed to grow to a maximum volume of 250 mm3, and the mice were subsequently treated daily at the indicated dose levels with CDK2/4 inhibitors by intraperitoneal injection in combination with a BRAFV600E- or MEK-inhibitor. CDK2/4 inhibitor (CVT-313/indolocarbazole CDK4-I) treatment sensitizes tumors to GDC-0879 and CI1040.

    J Natl Cancer Inst 2012 104(21), 1673-9. PD184352 (CI-1040) purchased from Selleck.

    LY294002 (10 μM for 12 h)- and PD184352 (10 μM for 12 h)-treated Her2-transfected DU145 and PC3 cells, respectively, showed reciprocal feedback inhibition between the PI3K/AKT and MEK/ERK path ways

    Proc Natl Acad Sci U S A 2011 108, 16392-7. PD184352 (CI-1040) purchased from Selleck.

  • a Expression and phosphorylation status of AKT and ERK1/2 and amount of cleaved CPP32 at 72 h after drug treatment were assessed by western blot. Actin was used to confirm equal protein loading. A representative experiment of three was reported. The panel shows cropped blots.

    J Hematol Oncol, 2017, 10(1):19. PD184352 (CI-1040) purchased from Selleck.

    The effect of CI-1040 on cell viability of molecular apocrine lines. MTT assay to measure cell viability in MDA-MB-453 cell line after treatment with CI-1040 (CI) at 2 to 25 μM concentrations. MTT assay to measure cell viability in HCC-1954 cell line after treatment with CI-1040 at 2 to 25 μM concentrations.

    Breast Cancer Res 2011 13, R36. PD184352 (CI-1040) purchased from Selleck.

  • Combination indices (CI) for flutamide (FLU) and CI-1040 combination therapy in MDA-MB-453-R line using MTT assay. Therapies were carried out with flutamide at 5 and 10 μM with each concentration of CI-1040 at 5 and 10 μM (CI-5 and CL-10). The concentrations of fluatmide and CI-1040 monotherapies with an effect similar to that of each combination therapy are depicted. Error bars: ±2SEM. Western blot analysis was used to measure the phosphorylated and total ERK levels in MDA-MB-453-R line following combination therapies with CI-1040 (5 μM)/flutamide (5 μM) and CI-1040 (5 μM)/flutamide (10 μM). RR values were measured relative to the untreated MDA-MB-453-R line.

    Breast Cancer Res 2011 13, R36. PD184352 (CI-1040) purchased from Selleck.

    Western blot analysis to measure the phosphorylated and total ERK levels in MDA-MB-453 and HCC-1954 cell lines after treatment with CI-1040 (CI) at 10-μM concentration.

     

     

    Neoplasia 2011 13, 154–166. PD184352 (CI-1040) purchased from Selleck.

  • Relative expression of AR using RT-PCR in MDA-MB-453 and HCC-1954 cell lines after treatment with CI-1040 (MEK Inh) at 10-μMconcentration for 24 hours. Expression is relative to that of vehicle-treated cells (CTL). *P < .01 is for CI-1040 versus control. Error bars,±2 SEMs.

     

     

    Neoplasia 2011 13, 154–166. PD184352 (CI-1040) purchased from Selleck.

    Synergistic effect of AR and mitogen-activated protein kinase kinase inhibitors on cell viability. (A) MTT assay to measure cell viability in MDA-MB-453 cell line after monotherapies and combination treatments with flutamide (FLU) and CI-1040 (CI) at 5 and 10 μΜ concentrations. CTL: control. Error bars: ±2 SEM. (B) Combination indices (CI) for flutamide and CI-1040 combination therapy in MDA-MB-453 cell line using MTT assay. Cell viability was measured after combination therapies with flutamide at 5 and 10 μM with each concentration of CI-1040 at 5 and 10 μM. The concentrations of FLU and CI-1040 monotherapies with an effect similar to that of each combination therapy are depicted. Error bars: ±2 SEM. (C) Combination indices for flutamide and CI-1040 combination therapy in HCC-1954 cell line using MTT assay. Cell viability was measured after combination therapies with flutamide at 20 and 40 μM with each concentration of CI-1040 at 5 and 10 μM. (D) Combination indices for flutamide and CI-1040 combination therapy in HCC-202 cell line using MTT assay at concentrations described in Figure 2C.

     

     

    Neoplasia 2011 13, 154–166. PD184352 (CI-1040) purchased from Selleck.

  • After starved in serum-free medium for 24h, Breast cancer cells incubated with the indicated concentrations of CI-1040 for 3h,followed by 15-minute stimulation of 100ng/ml EGF

     

     

    2010 Dr. Zhang of Tianjin Medical University. PD184352 (CI-1040) purchased from Selleck.

    After starved in serum-free medium for 24h, Breast cancer cells incubated with the indicated concentrations of CI-1040 for 3h,followed by 15-minute stimulation of 100ng/ml EGF

     

    2010 Dr. Zhang of Tianjin Medical University. PD184352 (CI-1040) purchased from Selleck.

  • The bar chart represents the relative numbers of third-round colonies of primary hematopoietic cells transduced with MLL-AF9 with treatment of compound PD184352 (CI-1040, 10 μM, a MEK inhibitor) and SB216763 (10 μM, GSK-3 inhibitor). The synergic effect between compounds CI-1040 and SB-216763 has been observed.

     

     

    2010 Dr. Shuo Dong of Baylor College of Medicine. PD184352 (CI-1040) purchased from Selleck.

Purity & Quality Control

Choose Selective MEK Inhibitors

Biological Activity

Description PD184352 (CI-1040) is an ATP non-competitive MEK1/2 inhibitor with IC50 of 17 nM in cell-based assays, 100-fold more selective for MEK1/2 than MEK5. Phase 2.
Features First MEK inhibitor to begin clinical development.
Targets
MEK1 [1]
(Cell-free assay)
MEK2 [1]
(Cell-free assay)
17 nM 17 nM
In vitro

CI-1040 treatment produces a reduction of pMAPK levels in multiple tumor cells including Colon 26, BX-PC3 pancreatic, A431 cervical, HT-29 colon, ZR-25-1 breast and SKOV-3 ovarian carcinomas. CI-1040 treatment doesn't inhibit the phosphorylation of Jun kinase, p38 kinase or Akt, indicating CI-1040 specifically targets MEK. Inhibition of MAPK activation by CI-1040 prevents cell cycle progression and induces a G1 block. [1] The IC50 for inhibition of MEK1 by CI-1040 is 0.3 μM, 15-fold higher than the concentration required to inhibit the EGF-induced activation of ERK2 in Swiss 3T3 cells. These results indicate CI-1040 exerts its effects on cells by suppressing the activation of MKK1, and not by blocking its activity. 2 nM PD184352 inhibits the activation of MKK1 in Swiss 3T3 cells by 50%, while over 100-fold concentration of CI-1040 inhibits MEK1 in vitro. PD184352 also inhibits the Raf-catalysed phosphorylation of MEK1 without any effect on the Raf-catalysed phosphorylation of myelin basic protein. [2] CI-1040 inhibits 86% of papillary thyroid carcinoma (PTC) cell growth with the RET/PTC1 rearrangement at 10μM compared with cells treated with DMSO only. CI-1040 shows potent inhibition to PTC cells (BRAF mutation) with GI50 of 52 nM, but low activity to RET/PTC1 rearrangement type with GI50 of 1.1 μM. [3] A recent research indicates CI-1040 increases the apoptotic effect of BMS-214662 in a CML blast crisis cell line, K562, and in primary chronic phase CD34+ CML cells. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
H9 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MYLJR|UxRTBwMEKyO|Yh|ryP NWHjcWl6W0GQR1XS
CHP-212 M4\RSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M1jtNmlEPTB;MD6wNlg5PSEQvF2= Ml3KV2FPT0WU
EoL-1-cell MUHHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIrCVJdKSzVyPUCuNFQyPTJizszN NVOxOWVbW0GQR1XS
DU-4475 MYXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NVXVXllXUUN3ME2wMlA4PTl7IN88US=> M2TUNXNCVkeHUh?=
MMAC-SF NFfhVVJIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2DId2lEPTB;MD6xNFk4PCEQvF2= NGjlenBUSU6JRWK=
AGS M3XNSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEXXfZRKSzVyPUCuNVE4OTNizszN MVLTRW5ITVJ?
M14 MV;Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NW\Ze5VkUUN3ME2wMlE2PDZ6IN88US=> NXq2VHo3W0GQR1XS
CP50-MEL-B M2\zZ2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MV7JR|UxRTBwMUeyOVQh|ryP M3XXb3NCVkeHUh?=
C32 M{nzeGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M3j5UWlEPTB;MD6xPVA4OiEQvF2= MnL0V2FPT0WU
KMOE-2 MoDwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHLFeIdKSzVyPUCuNVk4QTVizszN MYrTRW5ITVJ?
A101D MkLTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MWLJR|UxRTBwMkG0JO69VQ>? MWnTRW5ITVJ?
KM12 NI\GV2pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWTJR|UxRTBwMkSwOVch|ryP NH7MdmhUSU6JRWK=
HSC-4 M3PEN2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYTJR|UxRTBwMkSzPVUh|ryP M{jJRXNCVkeHUh?=
NOMO-1 M4OyUWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NWHC[HBwUUN3ME2wMlI2PzR{IN88US=> NFfnWWtUSU6JRWK=
MZ7-mel M4jFSGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MYjJR|UxRTBwMk[zOEDPxE1? NH\CeGJUSU6JRWK=
ACN MWjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NGDLW5ZKSzVyPUCuNlY4OzdizszN NVG4SHVQW0GQR1XS
MEL-HO NUG2eW1LT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NH64bo5KSzVyPUCuNlc3PTJizszN Ml;FV2FPT0WU
BHT-101 MV3Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MWPJR|UxRTBwMki2NFYh|ryP NHnVR5lUSU6JRWK=
SK-MEL-28 NYji[pBsT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MV\JR|UxRTBwM{C0NFkh|ryP NWD4b3QxW0GQR1XS
KG-1 MmO4S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MXjJR|UxRTBwM{C2Olgh|ryP M4roZ3NCVkeHUh?=
COLO-679 MnG0S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NV7yXGJpUUN3ME2wMlMzPzJizszN M2XxO3NCVkeHUh?=
SK-MEL-24 MmnTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEjhNZhKSzVyPUCuN|I5OTNizszN Ml3PV2FPT0WU
G-361 NHfi[IFIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NFfkVY1KSzVyPUCuN|Y4QTVizszN M3i2XHNCVkeHUh?=
KY821 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MlzUTWM2OD1yLkO3PVEh|ryP NWjaOXQ5W0GQR1XS
KASUMI-1 M4K0SWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NXjmOYxPUUN3ME2wMlM6QSEQvF2= M17QOXNCVkeHUh?=
HL-60 NHqwbVlIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NH7rdlZKSzVyPUCuOFEyODdizszN NIG0NWNUSU6JRWK=
K5 NUjGZpZKT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnHuTWM2OD1yLkSzNVE4KM7:TR?= MXzTRW5ITVJ?
KU812 MkTQS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYXyOVA4UUN3ME2wMlQ2Ojl7IN88US=> MlvoV2FPT0WU
SH-4 NU\ke|QyT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NVfXeHVKUUN3ME2wMlQ3OjV4IN88US=> NVrlUlJ2W0GQR1XS
HTC-C3 MoruS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NInFdnJKSzVyPUCuOFY2OzFizszN M{PjRnNCVkeHUh?=
CP66-MEL NEK1b5pIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M{\NbmlEPTB;MD60PFgxQSEQvF2= NYXpWVFLW0GQR1XS
WM-115 MkPxS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1q4N2lEPTB;MD60PVI2PyEQvF2= MXfTRW5ITVJ?
A2780 MYPHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MmXXTWM2OD1yLkS5PFI{KM7:TR?= NXW5XZNiW0GQR1XS
P12-ICHIKAWA NHrWeZhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NWLtepBzUUN3ME2wMlYyOjJzIN88US=> MV\TRW5ITVJ?
HMV-II NHzaW4xIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NF;TWFBKSzVyPUCuOlQ1PjVizszN M1jhfHNCVkeHUh?=
HT-144 M{Dmcmdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MoXYTWM2OD1yLk[0OlU4KM7:TR?= MorKV2FPT0WU
LB2518-MEL NEfvPJhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MnTmTWM2OD1yLkexOlMzKM7:TR?= M1zXdnNCVkeHUh?=
NCI-SNU-1 Mnf1S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIfDNZpKSzVyPUCuO|U1OzNizszN NWPvUpBRW0GQR1XS
C2BBe1 MlryS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7oNGxKSzVyPUCuPFExOjNizszN MXHTRW5ITVJ?
PSN1 NXvPSoFHT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NGjtXIJKSzVyPUCuPVYyQTZizszN MVvTRW5ITVJ?
UACC-257 NEnIN2hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MW\JR|UxRTBwOU[0O|Mh|ryP MnHqV2FPT0WU
RVH-421 NGTQNWNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M1fSd2lEPTB;MD65O|E5KM7:TR?= NELZeopUSU6JRWK=
GP5d M3XjV2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NH7GbGJKSzVyPUCuPVg{ODhizszN NILpfG5USU6JRWK=
TYK-nu NGfFNIhIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MWPJR|UxRTFwMEOxO|Ih|ryP MkPVV2FPT0WU
SK-N-AS MoDaS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M1HhU2lEPTB;MT6wO|k1PyEQvF2= MorYV2FPT0WU
SW620 MVnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NF\UZ2dKSzVyPUGuNVM2OzRizszN NXrY[IRmW0GQR1XS
HuP-T4 MUnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MX3JR|UxRTFwMUizOVkh|ryP NVLjcmdyW0GQR1XS
A549 NGPRT3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MoTsTWM2OD1zLkG5OVc3KM7:TR?= M4XJTXNCVkeHUh?=
Mewo NHjqZ41Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIi3W25KSzVyPUGuNlAzPzZizszN MX7TRW5ITVJ?
ONS-76 NILsXYNIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= Mm[zTWM2OD1zLkKyNFQ6KM7:TR?= NUj0[VRmW0GQR1XS
SK-MEL-1 MVLHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M2HzZWlEPTB;MT6yN|QyQSEQvF2= MoTWV2FPT0WU
RCM-1 MnPGS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NHf3d3BKSzVyPUGuNlQxPDdizszN M3\yVnNCVkeHUh?=
H-EMC-SS M3\UXGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEPHdJVKSzVyPUGuNlk3ODhizszN NH\Fd|VUSU6JRWK=
NCI-H2291 NX7ORY9WT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M4W2T2lEPTB;MT6zNlU{PiEQvF2= NVPsbo1PW0GQR1XS
SW1463 NHHYRmtIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUjJR|UxRTFwM{O3NlEh|ryP NVLRZ2Q6W0GQR1XS
LS-411N MlrTS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NF7m[WRKSzVyPUGuOFA2OTdizszN M1vvNXNCVkeHUh?=
BV-173 Ml\3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NYLVT2Q2UUN3ME2xMlQ1ODF3IN88US=> MlHqV2FPT0WU
LS-513 NHXySWxIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NUHj[mtvUUN3ME2xMlQ2OTl{IN88US=> M1nae3NCVkeHUh?=
LoVo M4DhW2dzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M2G3TWlEPTB;MT60OlM6QSEQvF2= MYXTRW5ITVJ?
HO-1-N-1 NGLJW|VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIXLTXBKSzVyPUGuOVE3OzRizszN MWTTRW5ITVJ?
ML-2 NYrUV5NmT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NFTVUmhKSzVyPUGuOVI5PjhizszN M2noS3NCVkeHUh?=
NCI-H1437 MoCwS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2TPWWlEPTB;MT61OVI4PSEQvF2= NGTOXW5USU6JRWK=
SW1116 MY\Hdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NYf3V|BjUUN3ME2xMlU3Ozl6IN88US=> Mn\JV2FPT0WU
A4-Fuk MkT3S5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M3S2NGlEPTB;MT61O|A1PSEQvF2= NUHlcnVRW0GQR1XS
HD-MY-Z NUPtcIRWT3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= NXjCUFdFUUN3ME2xMlU4Ozd4IN88US=> MlzqV2FPT0WU
SK-MEL-2 NFjTVY5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MUTJR|UxRTFwNUe0OVkh|ryP NULDXG1zW0GQR1XS
RT-112 NIXkT3hIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3nHVmlEPTB;MT61PFk2OiEQvF2= MWnTRW5ITVJ?
COLO-829 MUfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NUnNeXZSUUN3ME2xMlYzOjN{IN88US=> NHXLbHJUSU6JRWK=
OVCAR-5 M3fVNWdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NYPFNWhDUUN3ME2xMlc4Pjh5IN88US=> MkXpV2FPT0WU
NB69 NHTiUm5Iem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NGfoenpKSzVyPUGuO|g1PjlizszN NH;RdXpUSU6JRWK=
NCI-H292 MnvDS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? M2PKT2lEPTB;MT64OlY6QSEQvF2= MWrTRW5ITVJ?
LOXIMVI NIfSZlBIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= MX3JR|UxRTFwOEm0Nlch|ryP MmXUV2FPT0WU
BPH-1 MknCS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEjYUVdKSzVyPUGuPFk2QTFizszN MXnTRW5ITVJ?
A375 MYfHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUXJR|UxRTFwOEm3NVQh|ryP M{myeXNCVkeHUh?=
LCLC-97TM1 MXnHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? M1rQOWlEPTB;MT65NlI2PiEQvF2= MVrTRW5ITVJ?
RXF393 NIrrfFdIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= NIThZXFKSzVyPUGuPVc5QDdizszN Mn[yV2FPT0WU
HCC70 NYfBOFM6T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= M{fYd2lEPTB;Mj6wNlQzPiEQvF2= M3PKU3NCVkeHUh?=
EM-2 MorqS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NUfIbHI4UUN3ME2yMlA4OTl6IN88US=> NXvhfXB7W0GQR1XS
MZ2-MEL MUjHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? NIrh[I9KSzVyPUKuNVEyOjdizszN NYj5So53W0GQR1XS
HN M1z4SGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 M4rpZmlEPTB;Mj6xOlI4QCEQvF2= M1HRT3NCVkeHUh?=
A2058 MkXSS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnnDTWM2OD1{LkG5Nlc6KM7:TR?= MXnTRW5ITVJ?
NB7 NWi1c4E1T3Kxd4ToJGlvcGmkaYTpc44hSXO|YYm= MnfYTWM2OD1{LkO0NFg3KM7:TR?= NXnyT5dyW0GQR1XS
DOK M1\qWGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 NEnRc21KSzVyPUKuN|U4PzNizszN MVTTRW5ITVJ?
CAL-27 MorsS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NEPlSoJKSzVyPUKuN|kzOzZizszN Mlq3V2FPT0WU
BB65-RCC NF\rOFVIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M2rhemlEPTB;Mj60NFY4PCEQvF2= MU\TRW5ITVJ?
RD M2q2Umdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MkHGTWM2OD1{LkS0O|I{KM7:TR?= MmDqV2FPT0WU
KNS-62 MlPPS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NIPzcYdKSzVyPUKuOVEyPjRizszN MmHsV2FPT0WU
EW-13 MlHUS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? NID5fYFKSzVyPUKuOVY{OzlizszN MWHTRW5ITVJ?
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GCT M1\BUGdzd3e2aDDJcohq[mm2aX;uJGF{e2G7 MVvJR|UxRTF|Lkm2PVch|ryP MlLtV2FPT0WU
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BALL-1 MWXHdo94fGhiSX7obYJqfGmxbjDBd5NigQ>? MUPJR|UxRTF2LkS2OlUh|ryP MYrTRW5ITVJ?
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OVCAR-8 NGm5W5VIem:5dHigTY5pcWKrdHnvckBCe3OjeR?= M3OxcmlEPTB;MUSuO|IxOSEQvF2= MmLhV2FPT0WU
NCI-H2347 MlHIS5Jwf3SqIFnubIljcXSrb36gRZN{[Xl? MnnXTWM2OD1zND64NlMh|ryP NFjVU2JUSU6JRWK=
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... Click to View More Cell Line Experimental Data

In vivo Oral dosing of CI-1040 impairs the growth of colon tumor xenografts of mouse and human with a wide dose range of 48-200 mg/kg per dose, but not of P388 leukemia. [1] CI-1040 inhibits the tumor xenografts from PTC cells carrying a BRAF mutation with 31.3% reduction, carrying the RET/PTC1 rearrangement with 47.5% reduction than in untreated (vehicle) mice after 3 weeks of oral administration (300 mg/kg/d). No toxic effects are observed in any mice when they are treated with CI-1040. [2] Transient exposure of mammary tumors to CI-1040 and UCN-01 causes tumor cell death in vivo and prolonged suppression of tumor regrowth. Combined treatment with CI-1040 (25 mg/kg) and UCN-01 (0.1-0.2 mg/kg) significantly reduces MDA-MB-231, and largely abolishs MCF7 tumor growth in implanted athymic mice, while either single treatment has no significant activity. The drug combination leads to profound tumor cell death which correlates with a reduction in the phosphorylation of ERK1/2 and the immuno-reactivity of Ki67 and of CD31. [5]

Protocol

Kinase Assay:

[2]

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MEK1 Assay:

MAP kinase is activated after phosphorylation by MEK; the activated MAP kinase subsequently phosphorylates myelin basic protein (MBP).Incorporation of 32P into myelin basic protein (MBP) is assayed in the presence of glutathione S-transferase (GST) fusion proteins containing the 44-kDa MAPK (GST-MAPK) or the 45-kDa MEK (GST-MEK1). Assays are conducted in 50μL of 50 mM Tris, pH 7.4/10 mM MgCl2 /2 mM EGTA/10 μM [γ-32P]ATP containing 10 μg of GST-MEK1, 0.5 μg of GST-MAPK, and 40 μg of MBP. After incubation at 30°C for 15 minutes, reactions are stopped by addition of Laemmli SDS sample buffer. Phosphorylated MBP is resolved by SDS/10% PAGE. This screening effort leads to the discovery of several small-molecule inhibitors of MEK, i.e. CI-1040. Experiments assessing the order of addition shows that CI-1040 directly inhibits MEK1 with a 50% inhibitory concentration (IC50) of 17 nM, without affecting the activity of MAPK.
Cell Research:

[1]

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  • Cell lines: Colon 26 carcinoma cells
  • Concentrations: 0.1-10 μM
  • Incubation Time: 24 hours
  • Method:

    Cells are planted seeded in T-75 cm 2 flasks and treated the next day for 24 hous with either DMSO or CI-1040. Single-cell suspensions are collected, and pellets are fixed in ice-cold ethanol (70%) for 30 minutes. After centrifugation of the samples, propidium iodide (50 μg/mL) and RNase (30 units/mL) are added to the pellets for 20 minutes at 37 °C. After filtration, samples are analyzed by flow cytometry.


    (Only for Reference)
Animal Research:

[3]

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  • Animal Models: PTC cells in athymic mice
  • Formulation: Cremophor EL–95% ethanol (50:50) and dilutes with water
  • Dosages: 150 mg/kg
  • Administration: Orally twice daily
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 96 mg/mL (200.55 mM)
Ethanol 14 mg/mL (29.24 mM)
Water Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol, pH 9
For best results, use promptly after mixing.
10 mg/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 478.67
Formula

C17H14ClF2IN2O2

CAS No. 212631-79-3
Storage powder
in solvent
Synonyms N/A

Bio Calculators

Molarity Calculator

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)

  • Mass
    Concentration
    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
NCT00033384 Completed Breast Cancer|Colorectal Cancer|Lung Cancer|Pancreatic Cancer University of Alabama at Birmingham|National Cancer Institute (NCI) February 2002 Phase 2
NCT00034827 Completed Colorectal Neoplasms|Breast Neoplasms|Carcinoma, Non-Small-Cell Lung|Pancreatic Neoplasms Pfizer January 2002 Phase 2

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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MEK Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID