7t78 - Revision history

OCA at 13:07, 1 March 2024

OCA — Fri, 01 Mar 2024 13:07:26 GMT

←Older revision		Revision as of 13:07, 1 March 2024
Line 3:		Line 3:
	<StructureSection load='7t78' size='340' side='right'caption='[[7t78]], [[Resolution\|resolution]] 2.40Å' scene=''>		<StructureSection load='7t78' size='340' side='right'caption='[[7t78]], [[Resolution\|resolution]] 2.40Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[7t78]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7T78 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7T78 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7t78]] is a 2 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7T78 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7T78 FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=G2T:diethyl+{[2-(3-[4-(methanesulfonyl)phenoxy]-5-{[(2S)-1-methoxypropan-2-yl]oxy}benzamido)-1,3-thiazol-4-yl]methyl}phosphonate'>G2T</scene>, <scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene~~></td></tr>~~	+	</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models\|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution\|Resolution]] 2.4Å</td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Hexokinase Hexokinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.1 2.7.1.1] </span></td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=G2T:diethyl+{[2-(3-[4-(methanesulfonyl)phenoxy]-5-{[(2S)-1-methoxypropan-2-yl]oxy}benzamido)-1,3-thiazol-4-yl]methyl}phosphonate'>G2T</scene>, <scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7t78 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7t78 OCA], [https://pdbe.org/7t78 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7t78 RCSB], [https://www.ebi.ac.uk/pdbsum/7t78 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7t78 ProSAT]</span></td></tr>		<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7t78 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7t78 OCA], [https://pdbe.org/7t78 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7t78 RCSB], [https://www.ebi.ac.uk/pdbsum/7t78 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7t78 ProSAT]</span></td></tr>
	</table>		</table>
	== Disease ==		== Disease ==
-	[[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[https://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[https://omim.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>	+	[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[https://omim.org/entry/125851 125851]; also shortened MODY-2. MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[https://omim.org/entry/602485 602485]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>
	== Function ==		== Function ==
-	[[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.	+	[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	Glucokinase (GK) is a key regulator of glucose homeostasis, and its small-molecule activators represent a promising opportunity for the treatment of type 2 diabetes. Several GK activators have been advanced into clinical trials and have demonstrated promising efficacy; however, hypoglycemia represents a key risk for this mechanism. In an effort to mitigate this hypoglycemia risk while maintaining the efficacy of the GK mechanism, we have investigated a series of amino heteroaryl phosphonate benzamides as ''partial" GK activators. The structure-activity relationship studies starting from a "full GK activator" 11, which culminated in the discovery of the "partial GK activator" 31 (BMS-820132), are discussed. The synthesis and in vitro and in vivo preclinical pharmacology profiles of 31 and its pharmacokinetics (PK) are described. Based on its promising in vivo efficacy and preclinical ADME and safety profiles, 31 was advanced into human clinical trials.	+

-	Discovery of a Partial Glucokinase Activator Clinical Candidate: Diethyl ((3-(3-((5-(Azetidine-1-carbonyl)pyrazin-2-yl)oxy)-5-isopropoxybenzamido)-1H-pyra zol-1-yl)methyl)phosphonate (BMS-820132).,Shi Y, Wang Y, Meng W, Brigance RP, Ryono DE, Bolton S, Zhang H, Chen S, Smirk R, Tao S, Tino JA, Williams KN, Sulsky R, Nielsen L, Ellsworth B, Wong MKY, Sun JH, Leith LW, Sun D, Wu DR, Gupta A, Rampulla R, Mathur A, Chen BC, Wang A, Fuentes-Catanio HG, Kunselman L, Cap M, Zalaznick J, Ma X, Liu H, Taylor JR, Zebo R, Jones B, Kalinowski S, Swartz J, Staal A, O'Malley K, Kopcho L, Muckelbauer JK, Krystek SR Jr, Spronk SA, Marcinkeviciene J, Everlof G, Chen XQ, Xu C, Li YX, Langish RA, Yang Y, Wang Q, Behnia K, Fura A, Janovitz EB, Pannacciulli N, Griffen S, Zinker BA, Krupinski J, Kirby M, Whaley J, Zahler R, Barrish JC, Robl JA, Cheng PTW J Med Chem. 2022 Feb 18. doi: 10.1021/acs.jmedchem.1c02110. PMID:35179904<ref>PMID:35179904</ref>	+	==See Also==
-		+	*[[Hexokinase 3D structures\|Hexokinase 3D structures]]
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class~~=~~"pdbe-citations 7t78" style~~=~~"background-color:#fffaf0;"></div>~~	+
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Hexokinase~~]]	+	[[Category: Homo sapiens]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Muckelbauer~~, J K]]~~	+	[[Category: Muckelbauer JK]]
-	~~[[Category: Transferase~~]]	+

OCA at 12:01, 23 March 2022

OCA — Wed, 23 Mar 2022 12:01:40 GMT

←Older revision		Revision as of 12:01, 23 March 2022
Line 1:		Line 1:

	==CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-METHANESULFONYLPHENO XY)-5-{[(2S)-1-METHOXYPROPAN-2-YL]OXY}BENZAMIDO]-1,3-THIAZ OL-4-YL}METHYL)PHOSPHONATE==		==CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-METHANESULFONYLPHENO XY)-5-{[(2S)-1-METHOXYPROPAN-2-YL]OXY}BENZAMIDO]-1,3-THIAZ OL-4-YL}METHYL)PHOSPHONATE==
-	<StructureSection load='7t78' size='340' side='right'caption='[[7t78]]' scene=''>	+	<StructureSection load='7t78' size='340' side='right'caption='[[7t78]], [[Resolution\|resolution]] 2.40Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7T78 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7T78 FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[7t78]] is a 2 chain structure. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7T78 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7T78 FirstGlance]. <br>
-	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7t78 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7t78 OCA], [https://pdbe.org/7t78 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7t78 RCSB], [https://www.ebi.ac.uk/pdbsum/7t78 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7t78 ProSAT]</span></td></tr>	+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=EDO:1,2-ETHANEDIOL'>EDO</scene>, <scene name='pdbligand=G2T:diethyl+{[2-(3-[4-(methanesulfonyl)phenoxy]-5-{[(2S)-1-methoxypropan-2-yl]oxy}benzamido)-1,3-thiazol-4-yl]methyl}phosphonate'>G2T</scene>, <scene name='pdbligand=GLC:ALPHA-D-GLUCOSE'>GLC</scene>, <scene name='pdbligand=NA:SODIUM+ION'>NA</scene></td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[https://en.wikipedia.org/wiki/Hexokinase Hexokinase], with EC number [https://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.1 2.7.1.1] </span></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7t78 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7t78 OCA], [https://pdbe.org/7t78 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7t78 RCSB], [https://www.ebi.ac.uk/pdbsum/7t78 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7t78 ProSAT]</span></td></tr>
	</table>		</table>
		+	== Disease ==
		+	[[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:[https://omim.org/entry/125851 125851]]; also shortened MODY-2. MODY is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.<ref>PMID:1502186</ref> <ref>PMID:1464666</ref> <ref>PMID:1303265</ref> <ref>PMID:8495817</ref> <ref>PMID:8325892</ref> <ref>PMID:8446612</ref> <ref>PMID:8168652</ref> <ref>PMID:9049484</ref> <ref>PMID:10694920</ref> <ref>PMID:9662401</ref> <ref>PMID:10588527</ref> <ref>PMID:11106831</ref> <ref>PMID:11372010</ref> Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:[https://omim.org/entry/602485 602485]]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.<ref>PMID:9435328</ref>
		+	== Function ==
		+	[[https://www.uniprot.org/uniprot/HXK4_HUMAN HXK4_HUMAN]] Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	Glucokinase (GK) is a key regulator of glucose homeostasis, and its small-molecule activators represent a promising opportunity for the treatment of type 2 diabetes. Several GK activators have been advanced into clinical trials and have demonstrated promising efficacy; however, hypoglycemia represents a key risk for this mechanism. In an effort to mitigate this hypoglycemia risk while maintaining the efficacy of the GK mechanism, we have investigated a series of amino heteroaryl phosphonate benzamides as ''partial" GK activators. The structure-activity relationship studies starting from a "full GK activator" 11, which culminated in the discovery of the "partial GK activator" 31 (BMS-820132), are discussed. The synthesis and in vitro and in vivo preclinical pharmacology profiles of 31 and its pharmacokinetics (PK) are described. Based on its promising in vivo efficacy and preclinical ADME and safety profiles, 31 was advanced into human clinical trials.
		+
		+	Discovery of a Partial Glucokinase Activator Clinical Candidate: Diethyl ((3-(3-((5-(Azetidine-1-carbonyl)pyrazin-2-yl)oxy)-5-isopropoxybenzamido)-1H-pyra zol-1-yl)methyl)phosphonate (BMS-820132).,Shi Y, Wang Y, Meng W, Brigance RP, Ryono DE, Bolton S, Zhang H, Chen S, Smirk R, Tao S, Tino JA, Williams KN, Sulsky R, Nielsen L, Ellsworth B, Wong MKY, Sun JH, Leith LW, Sun D, Wu DR, Gupta A, Rampulla R, Mathur A, Chen BC, Wang A, Fuentes-Catanio HG, Kunselman L, Cap M, Zalaznick J, Ma X, Liu H, Taylor JR, Zebo R, Jones B, Kalinowski S, Swartz J, Staal A, O'Malley K, Kopcho L, Muckelbauer JK, Krystek SR Jr, Spronk SA, Marcinkeviciene J, Everlof G, Chen XQ, Xu C, Li YX, Langish RA, Yang Y, Wang Q, Behnia K, Fura A, Janovitz EB, Pannacciulli N, Griffen S, Zinker BA, Krupinski J, Kirby M, Whaley J, Zahler R, Barrish JC, Robl JA, Cheng PTW J Med Chem. 2022 Feb 18. doi: 10.1021/acs.jmedchem.1c02110. PMID:35179904<ref>PMID:35179904</ref>
		+
		+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
		+	</div>
		+	<div class="pdbe-citations 7t78" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
		+	[[Category: Hexokinase]]
	[[Category: Large Structures]]		[[Category: Large Structures]]
-	[[Category: Muckelbauer JK]]	+	[[Category: Muckelbauer, J K]]
		+	[[Category: Transferase]]

OCA at 06:22, 2 March 2022

OCA — Wed, 02 Mar 2022 06:22:28 GMT

←Older revision		Revision as of 06:22, 2 March 2022
Line 1:		Line 1:
-	'''Unreleased structure'''

-	~~The entry 7t78 is ON HOLD until Paper Publication~~	+	==CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-METHANESULFONYLPHENO XY)-5-{[(2S)-1-METHOXYPROPAN-2-YL]OXY}BENZAMIDO]-1,3-THIAZ OL-4-YL}METHYL)PHOSPHONATE==
-		+	<StructureSection load='7t78' size='340' side='right'caption='[[7t78]]' scene=''>
-	~~Authors: Muckelbauer, J.K.~~	+	== Structural highlights ==
-		+	<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=7T78 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=7T78 FirstGlance]. <br>
-	~~Description:~~ CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-METHANESULFONYLPHENO XY)-5-{[(2S)-1-METHOXYPROPAN-2-YL]OXY}BENZAMIDO]-1,3-THIAZ OL-4-YL}METHYL)PHOSPHONATE	+	</td></tr><tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=7t78 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=7t78 OCA], [https://pdbe.org/7t78 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=7t78 RCSB], [https://www.ebi.ac.uk/pdbsum/7t78 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=7t78 ProSAT]</span></td></tr>
-	[[Category: ~~Unreleased~~ Structures]]	+	</table>
-	[[Category: Muckelbauer~~, J.K~~]]	+	__TOC__
		+	</StructureSection>
		+	[[Category: Large Structures]]
		+	[[Category: Muckelbauer JK]]

OCA at 05:56, 19 January 2022

OCA — Wed, 19 Jan 2022 05:56:51 GMT

←Older revision		Revision as of 05:56, 19 January 2022
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 7t78 is ON HOLD	+	The entry 7t78 is ON HOLD until Paper Publication

	Authors: Muckelbauer, J.K.		Authors: Muckelbauer, J.K.

OCA: Protected "7t78" [edit=sysop:move=sysop]

OCA — Wed, 22 Dec 2021 14:08:04 GMT

Protected "7t78" [edit=sysop:move=sysop]

←Older revision

Revision as of 14:08, 22 December 2021

OCA: New page: '''Unreleased structure''' The entry 7t78 is ON HOLD Authors: Muckelbauer, J.K. Description: CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-MET...

OCA — Wed, 22 Dec 2021 14:08:01 GMT

New page: '''Unreleased structure''' The entry 7t78 is ON HOLD Authors: Muckelbauer, J.K. Description: CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-MET...

New page

'''Unreleased structure'''

The entry 7t78 is ON HOLD

Authors: Muckelbauer, J.K.

Description: CRYSTAL STRUCTURE OF GLUCOKINASE (HEXOKINASE 4) COMPLEXED WITH LIGAND DIETHYL ({2-[3-(4-METHANESULFONYLPHENO XY)-5-{[(2S)-1-METHOXYPROPAN-2-YL]OXY}BENZAMIDO]-1,3-THIAZ OL-4-YL}METHYL)PHOSPHONATE
[[Category: Unreleased Structures]]
[[Category: Muckelbauer, J.K]]