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- 저자 : 구교임(Kyo Im Koo) (검색결과 5 건)
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항암제인 Cyclophosphamide의 중간체인 $^{15}N$과 $^{17}O$-phosphoramide Mustards의 합성
구교임,염곤,Koo, Kyo-Im,Ryem, Kon 대한약학회 1994 약학회지 Vol.38 No.4
Each nitrogen and oxygen site isotope enriched the cyclophosphamide metabolite phosphoramide mustard was synthesized. Reaction of N,N-bis(2-chloroethyl)phosphoramidic dichloride$[Cl_2P(O)N(CH_2CH_2Cl)_2]$ with benzyl alcohol and ammonia gave N,N-bis(2-chloroethyl)phosphorodiamidic acid phenylmethyl ester $[BzO(H_2N)P(O)N(CH_2CH_2Cl)_2]$. Catalytic hydrogenation of this benzyl ester followed by the addition of cyclohexylamine provided PM. Incorporation of $^{15}NH_3$ into this general scheme gave PM with a $^{15}NH_2$ moiety. Glycine-$^{15}N$ was converted to bis(2-chloroethyl)amine-$^{15}N$ hydrochloride which, in turn, provided for N,N-bis(2-chloroethyl)phosphorodiamidic-$^{15}N$ dichloride. Use of this compound in the general synthetic pathway yielded PM CHA with $^{15}N$ in the mustard moiety. $^{17}O$-Enriched PM was generated through the use of benzyl alcohol-$^{17}O$. To obtain the alcohol, labelled benzaldehyde was made by exchange with $^{17}OH_2$ and was then reduced with sodium borohydride.
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항암제인 Cyclophosphamide의 중간체인 $^{15}N-Isophosphoramide$ Mustard에 관한 연구
구교임,염곤,Koo, Kyo-Im,Ryem, Kon 대한약학회 1994 약학회지 Vol.38 No.6
The each nitrogen site of ifosfamide metabolite isophosphoramide mustard was synthesized with isotope enriched nitrogen. $Gylcine-^{15}N$ was converted to $2-chloroethylamine-^{15}N$ hydrochloride which was then reacted with phenyl dichlorophosphate to provide $N,N'-bis(2-chloroethyl)phosphordiamidic-^{15}N_2$ acid phenylester(50%, $PhO(O)^{15}N(CH_2CH_2Cl_2)$. Catalytic hydrogenation of this phenyl ester followed by the addition of cyclohexylamine (CHA) provided $IPM-^{15}N$ as the CHA salt(70%).
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안영근(Young Keun Ahn),구자돈(Ja Don Koo),김정훈(Joung Hoon Kim),김봉희(Bong Hee Kim),조필형(Phil Hyoung Cho),구교임(Kyo Im Koo) 대한약학회 1992 약학회지 Vol.36 No.5
Effects of beta-carotene on the immunobiological responses were studied in ICR mice. ICR male mice were divided into 8 groups (10 mice/group), and beta-carotene at doses of 4, 20 and 100mg/kg were orally administered to ICR mice once daily for 28 consecutive days. Cyclophosphamide (CY) was injected intraperitoneally (i.p.) to ICR mice with a single dose of 5mg/kg body weight at 2 days before secondary immunization. Mice were sensitized and challenged with sheep red blood cells (S-RBC). Immune responses were evaluated by humoral immunity, cellular immunity and non-specific immunity. The results of this study were summarized as follows; (1) Beta-carotene significantly increased the weight ratios of liver, spleen and thymus to body weight depending on dose, and significantly increased the increasing rate of body weight and the number of circulating leukocyte. (2) Beta-carotene dose-dependently increased hemagglutination titer, Arthus reaction and hemolytic plaque forming cell related to humoral immunity. (3) Beta-carotene significantly increased delayed-type hypersensitivity reaction and rosette forming cell related to cellular immunity. (4) Beta-carotene dose-dependently increased phagocytic activity, and significantly increased natural killer (NK) cell activity. (5) Beta-carotene dose-dependently inhibited reductions in humoral immunity, cellular immunity, NK cell activity and phagocytic activity by treatment with CY.
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안영근,구자돈,김정훈,김봉희,조필형,구교임 충남대학교 약학대학 의약품개발연구소 1992 藥學論文集 Vol.8 No.-
Effects of beta-carotene on the immunobiological responses were studied in ICR mice. ICR male mice were divided into 8 groups (10 mice/group), and beta-carotene at doses of 4, 20 and 100 ㎎/㎏ were orally administered to ICR mice once daily for 28 consecutive days. Cyclophosphamide (CY) was injected intraperitoneally (i.p.) to ICR mice with a single dose of 5 ㎎/㎏ body weight at 2 days before secondary immunization. Mice were sensitized and challenged with sheep red blood cells (S-RBC). Immune responses were evaluated by humoral immunity, cellular immunity and non-specific immunity. The results of this study were summarized as follows; (1) Beta-carotene significantly increased the weight ratios of liver, spleen and thymus to body weight depending on dose, and significantly increased the increasing rate of body weight and the number of circulating leukocyte. (2) Beta-carotene dose-dependently increased hemagglutination titer, Arthus reaction and hemolytic plaque forming cell related to humoral immunity. (3)Beta-carotene significantly increased delayed-type hypersensitivity reaction and rosette forming cell relatted to cellular immunity. (4) Beta-carotene dose-dependently increased phagocytic activity, and significantly increased natural killer (NK) cell activity. (5) Beta-carotene dose-dependently inhibited reductions in humoral immunity, cellular immunity, NK cell activity and phagocytic activity by treatment with CY.
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안영근,구자돈,김정훈,김봉희,조필형,구교임 원광대학교 식품약품안전성연구소 1993 食品藥品安全性硏究 Vol.6 No.-
Effects of beta-carotene on the immunobiological responses were studied in ICR mice. ICR male mice were divided into 8 groups (10 mice/group), and beta-carotene at doses of 4, 20 and 100 ㎎/㎏ were orally administered to ICR mice once daily for 28 consecutive days. Cyclophosphamide (CY) was injected intraperitoneally (i.p.) to ICR mice with a single dose of 5 ㎎/㎏ body weight at 2 days before secondary immunization. Mice were sensitized and challenged with sheep red blood cells (S-RBC). Immune responses were evaluated by humoral immunity, cellular immunity and non-specific immunity. The results of this study were summarized as follows; (1) Beta-carotene significantly increased the weight ratios of liver, spleen and thymus to body weight depending on dose, and significantly increased the increasing rate of body weight and the number of circulating leukocyte. (2) Beta-carotene dose-dependently increased hemagglutination titer. Arthus reaction and hemolytic plaque forming cell related to humoral immunity. (3) Beta-carotene significantly increased delayed-type hypersensitivity reaction and rosette forming cell related to cellular immunity. (4) Beta-carotene dose-dependently increased phagocytic activity, and significantly increased natural killer (NK) cell activity. (5) Beta-carotene dose-dependently inhibited reductions in humoral immunity, cellular immunity, NK cell activity and phagocytic activity by treatment with CY.
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