https://scholar.dgist.ac.kr/handle/20.500.11750/10138 2026-04-07T17:41:44Z https://scholar.dgist.ac.kr/handle/20.500.11750/60155 Title: 코로나바이러스 감염증 COVID-19 치료용 펩타이드 및 이의 용도 Author(s): 이영호; 김민기; 권욱봉; 서소욱; 박송; 민가희; 이주환; 지상호; 장익수; 김상열; 유우경; 김효은; 최재석; 김희연; 박성준; 추효섭; 오명원; 이애리; 강무석; 이경은; 최성균; 최민지 Abstract: The present invention relates to a peptide for treatment of the corona virus infection COVID-19 and a use thereof. In order to make the binding to the new epitope of SARS-CoV2 RBD stronger compared to the peptide (P6) simulating the conventionally known binding site between SARS-CoV RBD and ACE2, the peptide of the present invention includes a new portion added with a novel amino acid sequence fundamentally designed for interaction in the dimension of atoms consisting of the amino acids. Suggested in the present invention is a novel design of a peptide having higher binding affinity than conventionally known peptides, wherein an expanded peptide is creatively designed to additionally interact with charged amino acids of D420 and K458, located at the rear side of the known binding boundary between RBD and hACE2. The peptide of the present invention exhibits high possibility as a therapeutic agent for COVID-19. https://scholar.dgist.ac.kr/handle/20.500.11750/60140 Title: CARS 현미경 및 이의 제어 방법 Author(s): 이관진; 김현민 Abstract: CARS 현미경이 개시된다. 본 CARS 현미경은 복수의 빔을 발생시키는 광원, 발생된 복수의 빔을 이용하여 중첩된 빔을 생성하는 이색 거울, 상기 중첩된 빔을 시료 내부로 집속하는 대물렌즈, 시료에서 발생된 CARS 신호의 사이드 로브(side lobes)를 제거하는 공초점 핀홀(confocal pinhole), 및 사이드 로브가 제거된 CARS 신호를 검출하는 광검출기를 포함한다. https://scholar.dgist.ac.kr/handle/20.500.11750/60085 Title: Effect of JIN-A02, a Novel 4Th-Generation EGFR-TKI, on Multiple EGFR Mutations in Comparison With 3Rd-Generation EGFR-TKIs Author(s): Lim, S- M.; Kim, Beom Soo; Yu, Wookyung; Choi, Seong-Kyoon; Jo, A.; Seah, E.; Kim, C.; Han, S.; Cho, B. C.; Kim, Hee-Yeon Abstract: JIN-A02, a novel fourth-generation tyrosine kinase inhibitor (TKI) targeting the epidermal growth factor receptor (EGFR) C797S mutation, is currently undergoing phase 1/2 clinical trials in patients with EGFR-mutated non-small cell lung cancer (NSCLC) in Korea, the USA, and Thailand (NCT05394831). NSCLC patients harboring acquired EGFR C797S mutations often exhibit co-occurring mutations, such as exon 19 deletions or T790M, as a result of targeted therapies, leading to tumor tissue heterogeneity. This heterogeneity significantly limits therapeutic options for these patients. To address this challenge, there is an unmet need for the development of fourth-generation EGFR-TKIs capable of targeting multiple EGFR mutations and effectively suppressing heterogeneous tumor tissues. With a view to evaluating the activity of JIN-A02 against common EGFR mutations (including T790M), we conducted an in silico study to estimate its binding affinity compared with third-generation EGFR-TKIs along with an in vitro study to calculate its inhibitory concentration (IC90) in EGFR-mutated cell lines. 2025-09-07T15:00:00Z https://scholar.dgist.ac.kr/handle/20.500.11750/59954 Title: Metixene hydrochloride hydrate mitigates kidney tubulointerstitial fibrosis by inhibiting Smad3 phosphorylation Author(s): Lee, Kyeong-Min; Hwang, Yeo Jin Abstract: Chronic Kidney disease (CKD), in which renal fibrosis is the defining pathological feature, poses significant global health and economic challenges. Despite its high clinical prevalence, effective therapies to prevent or reverse renal fibrosis remain scarce. Metixene hydrochloride hydrate (MHH), an anticholinergic drug once used for Parkinson's disease, has not been evaluated for renal fibrosis. Here, we investigated whether MHH mitigates renal fibrosis in a unilateral ureteral obstruction (UUO) mouse model and evaluated its effects on transforming growth factor-β1 (TGF-β1) signaling in renal cells. MHH did not affect the cell viability of NRK-49F cells at concentrations ranging from 0.5 to 5 μM. In vitro, MHH effectively suppressed TGF-β1-induced PAI-1 expression (both mRNA and protein) and secretion in renal fibroblasts, as well as PAI-1 secretion and protein expression in renal glomerular endothelial cells. Furthermore, TGF-β1 stimulated the mRNA and protein expressions of key renal fibrotic factors, including collagen type I, fibronectin, and alpha-smooth muscle actin, in NRK-49F cells. MMH significantly inhibited the expression of these renal fibrotic factors in these cells. UUO kidneys exhibited markedly increased tubular atrophy and interstitial fibrosis, as well as increased expression of renal fibrotic markers. MHH treatment significantly mitigated these pathological parameters and expression of renal fibrotic markers. Mechanistically, MHH suppressed TGF-β1-induced Smad3 phosphorylation both in vitro and in vivo. Our findings indicate that MHH exerts potent antifibrotic effects by downregulating the TGF-β1/Smad3 signaling pathway and suppressing the expression of fibrotic factors in renal cells and obstructed kidneys. Therefore, MHH could be repositioned as a therapeutic agent for renal fibrosis in various kidney diseases. 2026-02-28T15:00:00Z