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Dive into the research topics where Ji Yeon Song is active.

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Featured researches published by Ji Yeon Song.


International Journal of Cancer | 2012

Antitumor activity of HM781-36B, a highly effective pan-HER inhibitor in erlotinib-resistant NSCLC and other EGFR-dependent cancer models†

Mi Young Cha; Kwang-Ok Lee; Mi-Ra Kim; Ji Yeon Song; Kyu Hang Lee; Jongmin Park; Yun Jung Chae; Young Hoon Kim; Kwee Hyun Suh; Gwan Sun Lee; Seung Bum Park; Maeng Sup Kim

The epidermal growth factor receptor (EGFR) family of receptor tyrosine kinases has been implicated in a variety of cancers. In particular, activating mutations such as the L858R point mutation in exon 21 and the small in‐frame deletions in exon 19 of the EGFR tyrosine kinase domain are correlated with sensitivity to EGFR tyrosine kinase inhibitors in non‐small cell lung cancer (NSCLC) patients. Clinical treatment of patients is limited by the development of drug resistance resulting mainly from a gatekeeper mutation (T790M). In this study, we evaluated the therapeutic potential of a novel, irreversible pan‐HER inhibitor, HM781‐36B. The results from this study show that HM781‐36B is a potent inhibitor of EGFR in vitro, including the EGFR‐acquired resistance mutation (T790M), as well as HER‐2 and HER‐4, compared with other EGFR tyrosine kinases inhibitors (erlotinib, lapatinib and BIBW2992). HM781‐36B treatment of EGFR DelE746_A750‐harboring erlotinib‐sensitive HCC827 and EGFR L858R/T790M‐harboring erlotinib‐resistant NCI‐H1975 NSCLC cells results in the inhibition of EGFR phosphorylation and the subsequent deactivation of downstream signaling proteins. Additionally, HM781‐36B shows an excellent efficacy in a variety of EGFR‐ and HER‐2‐dependent tumor xenograft models, including erlotinib‐sensitive HCC827 NSCLC cells, erlotinib‐resistant NCI‐H1975 NSCLC cells, HER‐2 overexpressing Calu‐3 NSCLC cells, NCI‐N87 gastric cancer cells, SK‐Ov3 ovarian cancer cells and EGFR‐overexpressing A431 epidermoid carcinoma cancer cells. On the basis of these preclinical results, HM781‐36B is the most potent pan‐HER inhibitor, which will be advantageous for the treatment of patients with NSCLC including clinical limitation caused by acquired mutation (EGFR T790M), breast cancer and gastric cancer.


European Journal of Medicinal Chemistry | 2010

Pharmacophore modeling and virtual screening studies for new VEGFR-2 kinase inhibitors

Kyungik Lee; Ki-Woong Jeong; Yeon Joo Lee; Ji Yeon Song; Maeng Sup Kim; Gwan Sun Lee; Yangmee Kim

Virtual screening was performed to determine potent vascular endothelial growth factor receptor (VEGFR)-2 kinase inhibitors. A database of approximately 820,000 commercial compounds was used for screening, and 100 compounds were chosen as candidate VEGFR-2 inhibitors through pharmacophore modeling and docking studies. These 100 compounds were purchased to test their biological activities: 10 compounds were found to inhibit the enzyme, with IC(50) values ranging from 10 to 1 μM. Compound 1, which has a triazinoindole ring, inhibited the enzymatic activity of VEGFR-2, with an IC(50) value of about 1.6 μM, making it the most potent inhibitor of this enzyme. The triazinoindole derivative may therefore serve as the starting point in the design of new VEGFR-2 kinase inhibitors.


Journal of Medicinal Chemistry | 2009

Discovery of A Novel Her-1/Her-2 Dual Tyrosine Kinase Inhibitor for the Treatment of Her-1 Selective Inhibitor-Resistant Non-small Cell Lung Cancer

Mi Young Cha; Kwang-Ok Lee; Jong Woo Kim; Chang Gon Lee; Ji Yeon Song; Young Hoon Kim; Gwan Sun Lee; Seung Bum Park; Maeng Sup Kim

A novel series of (S)-1-acryloyl-N-[4-(arylamino)-7-(alkoxy)quinazolin-6-yl]pyrrolidine-2-carboxamides were synthesized and evaluated as Her-1/Her-2 dual inhibitors. In contrast to the Her-1 selective inhibitors, our novel compounds are irreversible inhibitors of Her-1 and Her-2 tyrosine kinases with the potential to overcome clinically relevant, mutation-induced drug resistance. The selected compounds (19c, 19d) showed excellent EGFR inhibition activity even toward the T790M mutation of Her-1 tyrosine kinase with excellent selectivity. The excellent pharmacokinetic profiles of these compounds in rats and their robust in vivo efficacy in an A431 xenograft model clearly demonstrate that they merit further investigation as novel therapeutic agents for EGFR-targeting treatment of solid tumors, especially Her-1 selective inhibitor-resistant non-small cell lung cancer.


Journal of Medicinal Chemistry | 2012

Synthesis and biological evaluation of pyrimidine-based dual inhibitors of human epidermal growth factor receptor 1 (HER-1) and HER-2 tyrosine kinases.

Mi Young Cha; Kwang-Ok Lee; SeokJong Kang; Young Hee Jung; Ji Yeon Song; Kyung Jin Choi; Joo Yun Byun; Hanjae Lee; Gwan Sun Lee; Seung Bum Park; Maeng Sup Kim

A novel series of N(4)-(3-chlorophenyl)-5-(oxazol-2-yl)pyrimidine-4,6-diamines were synthesized and evaluated as dual inhibitors of HER-1/HER-2 tyrosine kinases. In contrast to the currently approved HER-2-targeted agent (lapatinib, 1), our irreversible HER-1/HER-2 inhibitors have the potential to overcome the clinically relevant and mutation-induced drug resistance. The selected compound (19a) showed excellent inhibitory activity toward HER-1/HER-2 tyrosine kinases with selectivity over 20 other kinases and inhibited the proliferation of both cancer cell types: lapatinib-sensitive cell lines (SK-Br3, MDA-MB-175, and N87) and lapatinib-resistant cell lines (MDA-MB-453, H1781, and H1975). The excellent pharmacokinetic profiles of 19a in mice and rats led us to further investigation of a novel therapeutic agent for HER-2-targeting treatment of solid tumors, especially HER-2-positive breast/gastric cancer and HER-2-mutated lung cancer.


Cancer Research | 2014

Abstract LB-100: Discovery of HM61713 as an orally available and mutant EGFR selective inhibitor

Kwang-Ok Lee; Mi Young Cha; Mi-Ra Kim; Ji Yeon Song; Jaeho Lee; Young Hoon Kim; Young-Mi Lee; Kwee Hyun Suh; Jeewoong Son

Introduction: Activating mutations of EGFR are well known as oncogenic driver mutations in lung adenocarcinoma. Currently, EGFR TKIs including Gefitinib and Erlotinib are used as the first line therapy in NSCLC patients harboring EGFR activating mutations. However, drug resistance caused by T790M mutation limits the efficacy of these 1st generation EGFR TKIs. Currently, some of the next generation EGFR TKIs are under investigation for the treatment of lung cancer patients having T790M mutation. In our current presentation, to obtain HM61713, an EGFR mutant selective inhibitor, as a clinical candidate and the evaluation of HM61713 for mutant EGFR cancer model will be introduced. Method: Novel analogues were designed and synthesized to find active compounds for the T790M mutation as well as EGFR activating mutations with good selectivity over wild- type EGFR. Finally, HM61713 was selected as a clinical candidate through multi-optimization processes including both in vitro and in vivo pharmacologcal studies. Results: HM61713 was designed as an irreversible kinase inhibitor having a Michael acceptor, which covalently binds to a cysteine residue near the kinase domain of mutant the EGFR. In a cell wash out test, HM61713 inhibited phospho-EGFR for a long duration with a half-life of over 24 hours. From in vitro study, HM61713 showed potent activities for H1975 (L858-T790M) and HCC827 (exon 19 del.) with GI50 values of 9.2 nM and 10 nM, respectively. Instead, it showed low potency for H358 (wild type EGFR NSCLC) with GI50 of 2,225 nM. In xenograft studies using H1975 and HCC827, HM61713 resulted in good efficacy without showing any side effects. Conclusion: HM61713 showed excellent in vitro and in vivo activities for H1975 harboring L858R-T790M mutation as well as HCC827 having exon 19 deletion mutation with selectivity over wild-type EGFR. Currently, HM61713 is undergoing phase I study (NCT01588145) for NSCLC patients after the failure of 1st generation EGFR TKIs in Korea. Citation Format: Kwang-Ok Lee, Mi Young Cha, Mira Kim, Ji Yeon Song, Jae-Ho Lee, Young Hoon Kim, Young-Mi Lee, Kwee Hyun Suh, Jeewoong Son. Discovery of HM61713 as an orally available and mutant EGFR selective inhibitor. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-100. doi:10.1158/1538-7445.AM2014-LB-100


IEEE Transactions on Magnetics | 1998

Soft Magnetic Properties Of As-deposited Fe-Hf-C-N and Fe-Hf-N nanocrystalline thin films

Ji Yeon Song; J. Kim; H.J. Kim; Jun-kyoung Lee

143 WEDNESDAY MORNING, JANUARY 7, 1998 CONCOURSE, 9:00 TO 12:OO Session CU SOFT THIN FILMS (POSTER SESSION) Winston Win, Chair University of Texas, PRC-MER 1.203 R8625, Austin, TX 78712


Cancer Research | 2015

Abstract 2607: Antitumor activity of the selective RAF inhibitor HM95573 in solid tumors and hematologic malignancies

Young-Mi Lee; InHwan Bae; Namgoong Gwang Mo; Jaeho Lee; Su-Hyeon Kim; Ji Yeon Song; Kyu Hang Lee; Tae Hun Song; Young Gil Ahn; Young Hoon Kim; Kwee Hyun Suh

The mitogen-activated protein kinase (MAPK) pathway is particularly important for the survival and proliferation of tumor cells. Activation of the MAPK pathway due to mutations in BRAF, NRAS and KRAS is considered one of the causes of solid tumors (NSCLC, CRC,HCC, andthyroid cancers) and hematologic malignancies. HM95573 is a novel, highly potent RAF kinase inhibitor. Biochemically assayed for over 120 kinases, HM95573 showed the high selectivity toward BRAF mutant and CRAF kinases. The half maximal inhibition concentrations (IC50) of HM95573 against BRAFWT, BRAFV600E and CRAF kinases were 41nM, 7nM and 2nM, respectively. The strongly inhibited kinases subsequent to RAF kinases appeared to be CSF1R (44nM), DDR1 (77nM) and DDR2 (182 nM). HM95573 potently inhibited the growth of BRAFmutation CRC cell lines (e.g. IC50: 118nM for Colo-205) and thyroid cancer cell lines (43nM for B-CPAP); KRAS mutation NSCLC cell lines(297nM for Calu-6),CRC cell lines(65nM for HCT-116) and thyroid cancer cell lines(479nM for CAL-62); and NRAS mutation HCC cell lines(28nM for HepG2) andleukemia cell lines (39nM for HL-60). HM95573 effectively inhibited the phosphorylations of MEK and ERK, downstream kinases associated with cell proliferation in tumor cell lines mutated in BRAF, KRAS and NRAS. In addition, the phosphorylation of downstream kinases of RAF such as MEK and ERK was effectively inhibited with treatment of HM95573 in mutant KRAS NSCLC and CRC cells. HM95573 showed the excellent antitumor activity in mouse models xenografted with BRAF mutation cell line (Colo-205), KRAS mutation cell lines (Calu-6 and HCT-116)and NRAS mutation cell line (HepG2)two RAF inhibitors approved in melanoma which were effective to only BRAF mutation cell lines under conditions tested. The in vivo antitumor activity of HM95573 was potentiated with MEK inhibitors. Now, HM95573 is currently in phase I development in patients with advanced solid tumors including KRAS mutation NSCLC in Korea. Citation Format: Young-Mi Lee, InHwan Bae, Namgoong Gwang Mo, Jae Ho Lee, Suhyeon Kim, Ji Yeon Song, Kyu Hang Lee, Tae Hun Song, Young Gil Ahn, Young Hoon Kim, Kwee Hyun Suh. Antitumor activity of the selective RAF inhibitor HM95573 in solid tumors and hematologic malignancies. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2607. doi:10.1158/1538-7445.AM2015-2607


Archive | 2005

Quinazoline derivatives for inhibiting cancer cell growth and method for the preparation thereof

Young Jin Ham; Ji Hyeon Gong; Mi Young Cha; Jong-Woo Kim; Maeng Sup Kim; Eun Young Kim; Ji Yeon Song; Chang In Kim; Se Young Kim; Gwan Sun Lee


Bioorganic & Medicinal Chemistry | 2009

Structure-based virtual screening of Src kinase inhibitors

Kyungik Lee; Jong-Woo Kim; Ki-Woong Jeong; Ki Won Lee; Yeon Joo Lee; Ji Yeon Song; Maeng Sup Kim; Gwan Sun Lee; Yangmee Kim


Archive | 2011

THIENO[3,2-d]PYRIMIDINE DERIVATIVES HAVING INHIBITORY ACTIVITY ON PROTEIN KINASES

Jung Beom Son; Seung Hyun Jung; Wha Il Choi; Young Hee Jung; Jae Yul Choi; Ji Yeon Song; Kyu Hang Lee; Jae Chul Lee; Eun Young Kim; Young Gil Ahn; Maeng Sup Kim; Hwan Geun Choi; Tae Bo Sim; Young Jin Ham; Dong-Sik Park; Hwan Kim; Dong-Wook Kim

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Maeng Sup Kim

Korea Institute of Science and Technology

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Gwan Sun Lee

Korea Institute of Science and Technology

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Mi Young Cha

Seoul National University

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Young Hoon Kim

Seoul National University

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Eun Young Kim

Korea Institute of Science and Technology

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Seung Bum Park

Seoul National University

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Young Jin Ham

Korea Institute of Science and Technology

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Kwee Hyun Suh

Korea Institute of Science and Technology

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Kyu Hang Lee

Korea Institute of Science and Technology

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