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Kyung Ho Yoo - One of the best experts on this subject based on the ideXlab platform.
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synthesis of quinolinylaminopyrimidines and quinazolinylmethylaminopyrimidines with antiproliferative activity against Melanoma Cell Line
Journal of Enzyme Inhibition and Medicinal Chemistry, 2015Co-Authors: Jun A Lee, So Ha Lee, Taebo Sim, Eun Joo Roh, Jong Seung Kim, Kyung Ho YooAbstract:AbstractSynthesis of a new series of quinolinylaminopyrimidines 1a–k and quinazolinylmethylaminopyrimidines 2a–i containing aminoquinoLine and aminoquinazoLine as hinge regions is described. Their in vitro antiproliferative activities against A375P human Melanoma Cell Line were tested. Among them, compounds 1h and 1k exhibited the highest antiproliferative activities against A375P Cell Line with IC50 values in sub-micromolar scale. Compounds 1i, 2b and 2g showed similar potency against A375P to Sorafenib as a reference compound. The representative compound 1h showed high, dose-dependent inhibition of MEK and ERK kinases.
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synthesis of new pyrimidinylaminobenzene derivatives and their antiproliferative activities against Melanoma Cell Line
ChemInform, 2013Co-Authors: Hee Jin Kim, Kyung Ho YooAbstract:Diaryl amide (I) and diaryl urea (II) derivatives possessing a pyrimidinylaminobenzene scaffold are synthesized and some of them are screened for their in vitro antiproliferative activities against A375P human Melanoma Cell Line.
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synthesis of new pyrimidinylaminobenzene derivatives and their antiproliferative activities against Melanoma Cell Line
Bulletin of The Korean Chemical Society, 2013Co-Authors: Hee Jin Kim, Kyung Ho YooAbstract:Center for Biomaterials, Korea Institute of Science and Technology, P.O. Box 131, Cheongryang, Seoul 130-650, KoreaReceived April 15, 2013, Accepted May 7, 2013A series of new diarylamide and diarylurea derivatives possessing pyrimidinylaminobenzene scaffold wassynthesized. Their in vitro antiproliferative activities were tested against A375P human Melanoma Cell Line.Among them, compounds 1a-c, k and 2b-d, f, g, j, l showed superior potencies against A375P humanMelanoma Cell Line to Sorafenib. In particular, compound 2f possessing 3-fluoro-5-trifluoromethyl moietyexhibited the highest potency with IC
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synthesis and antiproliferative activity of new aminoisoquinolinylurea derivatives against Melanoma Cell Line
Bulletin of The Korean Chemical Society, 2012Co-Authors: Hye Jung Cho, So Ha Lee, Mohammed I Elgamal, Hong Seok Choi, Jun Hee Hong, Garam Kim, Kyung Ho YooAbstract:A series of new diarylureas possessing aminoisoquinoLine scaffold was synthesized, and their in vitro antiproliferative activity against A375P human Melanoma Cell Line was tested. Compounds 1d, 1l, 1n, 1p, 1q, and 1t showed superior potency against A375P to Sorafenib. The highest potency was shown by compound 1p possessing 3,5-bis(trifluoromethyl)phenyl terminal ring with IC50 value of 0.41 µM.
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new diarylureas and diarylamides possessing acet benz amidophenyl scaffold design synthesis and antiproliferative activity against Melanoma Cell Line
Bioorganic & Medicinal Chemistry Letters, 2012Co-Authors: Hee Jin Kim, Hwan Kim, So Ha Lee, Taebo Sim, Jungmi Hah, Mohammed I Elgamal, Hye Jung Cho, Kyung Ho YooAbstract:A series of new diarylurea and diarylamide derivatives possessing acet(benz)amidophenyl scaffold was synthesized. Their in vitro antiproliferative activity was tested against A375P human Melanoma Cell Line. Compounds 1c,d and 2c,d showed the highest potencies with IC(50) values in sub-micromolar scale. In addition, compounds 1b,e,l and 2e,l were more potent than Sorafenib but with IC(50) values in micromolar range. Moreover, compound 2c was equipotent to Vemurafenib, and 2d showed higher potency than Vemurafenib against A375P. Molar refractometry calculation and ADME profiling of the highest potent four derivatives 1c,d and 2c,d are also reported.
Mohammed I Elgamal - One of the best experts on this subject based on the ideXlab platform.
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synthesis and antiproliferative activity of new aminoisoquinolinylurea derivatives against Melanoma Cell Line
Bulletin of The Korean Chemical Society, 2012Co-Authors: Hye Jung Cho, So Ha Lee, Mohammed I Elgamal, Hong Seok Choi, Jun Hee Hong, Garam Kim, Kyung Ho YooAbstract:A series of new diarylureas possessing aminoisoquinoLine scaffold was synthesized, and their in vitro antiproliferative activity against A375P human Melanoma Cell Line was tested. Compounds 1d, 1l, 1n, 1p, 1q, and 1t showed superior potency against A375P to Sorafenib. The highest potency was shown by compound 1p possessing 3,5-bis(trifluoromethyl)phenyl terminal ring with IC50 value of 0.41 µM.
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new diarylureas and diarylamides possessing acet benz amidophenyl scaffold design synthesis and antiproliferative activity against Melanoma Cell Line
Bioorganic & Medicinal Chemistry Letters, 2012Co-Authors: Hee Jin Kim, Hwan Kim, So Ha Lee, Taebo Sim, Jungmi Hah, Mohammed I Elgamal, Hye Jung Cho, Kyung Ho YooAbstract:A series of new diarylurea and diarylamide derivatives possessing acet(benz)amidophenyl scaffold was synthesized. Their in vitro antiproliferative activity was tested against A375P human Melanoma Cell Line. Compounds 1c,d and 2c,d showed the highest potencies with IC(50) values in sub-micromolar scale. In addition, compounds 1b,e,l and 2e,l were more potent than Sorafenib but with IC(50) values in micromolar range. Moreover, compound 2c was equipotent to Vemurafenib, and 2d showed higher potency than Vemurafenib against A375P. Molar refractometry calculation and ADME profiling of the highest potent four derivatives 1c,d and 2c,d are also reported.
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new imidazo 2 1 b thiazole derivatives synthesis in vitro anticancer evaluation and in silico studies
ChemInform, 2012Co-Authors: Jin Hun Park, Mohammed I Elgamal, Yong Sup LeeAbstract:Compounds (IIIb), (IIIf), (IVb), and (IVd)—(IVg) exhibit higher activity against A375P human Melanoma Cell Line than the reference compound sorafenib.
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new diarylureas and diarylamides containing 1 3 4 triarylpyrazole scaffold synthesis antiproliferative evaluation against Melanoma Cell Lines erk kinase inhibition and molecular docking studies
ChemInform, 2012Co-Authors: Won Kyoung Choi, Mohammed I Elgamal, Hong Seok Choi, Daejin BaekAbstract:Derivatives (Ib)—(Id), and (IIIa)—(IIIc) show the highest potency against A375P human Melanoma Cell Line.
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design synthesis and antiproliferative activity of 3 4 diarylpyrazole 1 carboxamide derivatives against Melanoma Cell Line
ChemInform, 2012Co-Authors: Hong Seok Choi, Mohammed I Elgamal, Haeguk Cho, Jun Hee Hong, Kyung Ho YooAbstract:The title compounds (III) and (IV) are screened for their antiproliferative activity against the A375 human Melanoma Cell Line.
Michio Sata - One of the best experts on this subject based on the ideXlab platform.
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Cell cycle regulation by the wee1 inhibitor pd0166285 pyrido 2 3 d pyimidine in the b16 mouse Melanoma Cell Line
BMC Cancer, 2006Co-Authors: Osamu Hashimoto, Masako Shinkawa, Takuji Torimura, Toru Nakamura, Karuppaiyah Selvendiran, Masaharu Sakamoto, Hironori Koga, Takato Ueno, Michio SataAbstract:Background Wee1 kinase plays a critical role in maintaining G2 arrest through its inhibitory phosphorylation of cdc2. In previous reports, a pyridopyrimidine molecule PD0166285 was identified to inhibit Wee1 activity at nanomolar concentrations. This G2 checkpoint abrogation by PD0166285 was demonstrated to kill cancer Cells, there at a toxic highest dose of 0.5 μM in some Cell Lines for exposure periods of no longer than 6 hours. The deregulated Cell cycle progression may have ultimately damaged the cancer Cells. We herein report one of the mechanism by which PD0166285 leads to Cell death in the B16 mouse Melanoma Cell Line.
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Cell cycle regulation by the wee1 inhibitor pd0166285 pyrido 2 3 d pyimidine in the b16 mouse Melanoma Cell Line
BMC Cancer, 2006Co-Authors: Osamu Hashimoto, Masako Shinkawa, Takuji Torimura, Toru Nakamura, Karuppaiyah Selvendiran, Masaharu Sakamoto, Hironori Koga, Takato Ueno, Michio SataAbstract:Wee1 kinase plays a critical role in maintaining G2 arrest through its inhibitory phosphorylation of cdc2. In previous reports, a pyridopyrimidine molecule PD0166285 was identified to inhibit Wee1 activity at nanomolar concentrations. This G2 checkpoint abrogation by PD0166285 was demonstrated to kill cancer Cells, there at a toxic highest dose of 0.5 μM in some Cell Lines for exposure periods of no longer than 6 hours. The deregulated Cell cycle progression may have ultimately damaged the cancer Cells. We herein report one of the mechanism by which PD0166285 leads to Cell death in the B16 mouse Melanoma Cell Line. Tumor Cell proliferation was determined by counting Cell numbers. Cell cycle distribution was determined by flow cytometry. Morphogenesis analysis such as microtubule stabilization, Wee1 distribution, and cyclin B location were observed by immunofluorescence confocal microscopy. An immunoblot analysis of cdc2-Tyr15, cyclin D, E, p16, 21, 27, and Rb. A real-time PCR of the mRNA of cyclin D were completed. In our experiment, B16 Cells also dramatically abrogated the G2 checkpoint and were found to arrest in the early G1 phase by treatment with 0.5 μM for 4 hours observed by flow cytometry. Cyclin D mRNA decreased within 4 hours observed by Real-time PCR. Rb was dephosphrylated for 24 hours. However, B16 Cells did not undergo Cell death after 0.5 μM treatment for 24 hours. Immnofluoscence microscopy showed that the Cells become round and small in the morphogenesis. More interesting phenomena were that microtubule stabilization was blocked, and Wee1 distribution was restricted after treatment for 4 hours. We analyzed the effect of Wee1 inhibitor PD0166285 described first by Wang in the G2 transition in the B16 Melanoma Cell Line. The inhibitor PD0166285 abrogated G2/M checkpoint inducing early Cell division. Moreover, we found that the treatment of Cells with the inhibitor is related to microtubule stabilization and decrease in cyclin D transcription. These effects together suggest that Wee1 inhibitor may thus be a potentially useful anti-cancer therapy.
Osamu Hashimoto - One of the best experts on this subject based on the ideXlab platform.
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Cell cycle regulation by the wee1 inhibitor pd0166285 pyrido 2 3 d pyimidine in the b16 mouse Melanoma Cell Line
BMC Cancer, 2006Co-Authors: Osamu Hashimoto, Masako Shinkawa, Takuji Torimura, Toru Nakamura, Karuppaiyah Selvendiran, Masaharu Sakamoto, Hironori Koga, Takato Ueno, Michio SataAbstract:Background Wee1 kinase plays a critical role in maintaining G2 arrest through its inhibitory phosphorylation of cdc2. In previous reports, a pyridopyrimidine molecule PD0166285 was identified to inhibit Wee1 activity at nanomolar concentrations. This G2 checkpoint abrogation by PD0166285 was demonstrated to kill cancer Cells, there at a toxic highest dose of 0.5 μM in some Cell Lines for exposure periods of no longer than 6 hours. The deregulated Cell cycle progression may have ultimately damaged the cancer Cells. We herein report one of the mechanism by which PD0166285 leads to Cell death in the B16 mouse Melanoma Cell Line.
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Cell cycle regulation by the wee1 inhibitor pd0166285 pyrido 2 3 d pyimidine in the b16 mouse Melanoma Cell Line
BMC Cancer, 2006Co-Authors: Osamu Hashimoto, Masako Shinkawa, Takuji Torimura, Toru Nakamura, Karuppaiyah Selvendiran, Masaharu Sakamoto, Hironori Koga, Takato Ueno, Michio SataAbstract:Wee1 kinase plays a critical role in maintaining G2 arrest through its inhibitory phosphorylation of cdc2. In previous reports, a pyridopyrimidine molecule PD0166285 was identified to inhibit Wee1 activity at nanomolar concentrations. This G2 checkpoint abrogation by PD0166285 was demonstrated to kill cancer Cells, there at a toxic highest dose of 0.5 μM in some Cell Lines for exposure periods of no longer than 6 hours. The deregulated Cell cycle progression may have ultimately damaged the cancer Cells. We herein report one of the mechanism by which PD0166285 leads to Cell death in the B16 mouse Melanoma Cell Line. Tumor Cell proliferation was determined by counting Cell numbers. Cell cycle distribution was determined by flow cytometry. Morphogenesis analysis such as microtubule stabilization, Wee1 distribution, and cyclin B location were observed by immunofluorescence confocal microscopy. An immunoblot analysis of cdc2-Tyr15, cyclin D, E, p16, 21, 27, and Rb. A real-time PCR of the mRNA of cyclin D were completed. In our experiment, B16 Cells also dramatically abrogated the G2 checkpoint and were found to arrest in the early G1 phase by treatment with 0.5 μM for 4 hours observed by flow cytometry. Cyclin D mRNA decreased within 4 hours observed by Real-time PCR. Rb was dephosphrylated for 24 hours. However, B16 Cells did not undergo Cell death after 0.5 μM treatment for 24 hours. Immnofluoscence microscopy showed that the Cells become round and small in the morphogenesis. More interesting phenomena were that microtubule stabilization was blocked, and Wee1 distribution was restricted after treatment for 4 hours. We analyzed the effect of Wee1 inhibitor PD0166285 described first by Wang in the G2 transition in the B16 Melanoma Cell Line. The inhibitor PD0166285 abrogated G2/M checkpoint inducing early Cell division. Moreover, we found that the treatment of Cells with the inhibitor is related to microtubule stabilization and decrease in cyclin D transcription. These effects together suggest that Wee1 inhibitor may thus be a potentially useful anti-cancer therapy.
Ulrich Lehmann - One of the best experts on this subject based on the ideXlab platform.
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mda mb 435 the questionable use of a Melanoma Cell Line as a model for human breast cancer is ongoing
Cancer Biology & Therapy, 2007Co-Authors: Matthias Christgen, Ulrich LehmannAbstract:In September 2006, Rae et al. provided unmistakable evidence that the MDA-MB-435 human breast cancer Cell Line is identical to the M14 human Melanoma Cell Line. This discovery was no surprise to the breast cancer research community. In fact, the expression of melanocyte specific marker proteins by MDA MB-435 Cells was first recognized many years ago. In 2007, the year after MDA-MB-435 Cells were officially redefined as Melanoma Cells, this mix-up has gained a new aspect: We could easily identify 20 novel studies published in the recent issues of leading journals which simply proceeded to employ MDA-MB-435 Cells as a model system for human breast cancer. Here we want to draw attention to this questionable practice which should further raise our (self-) skepticism and awareness about the true origin, the identity and molecular properties of any biological materials used in cancer research.