5vlr - Revision history

OCA at 14:11, 13 March 2024

OCA — Wed, 13 Mar 2024 14:11:12 GMT

←Older revision		Revision as of 14:11, 13 March 2024
Line 1:		Line 1:

	==CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR==		==CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR==
-	<StructureSection load='5vlr' size='340' side='right' caption='[[5vlr]], [[Resolution\|resolution]] 2.80Å' scene=''>	+	<StructureSection load='5vlr' size='340' side='right'caption='[[5vlr]], [[Resolution\|resolution]] 2.80Å' scene=''>
	== Structural highlights ==		== Structural highlights ==
-	<table><tr><td colspan='2'>[[5vlr]] is a 2 chain structure with sequence from [~~http~~://en.wikipedia.org/wiki/~~Human Human~~]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5VLR OCA]. For a <b>guided tour on the structure components</b> use [~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5VLR FirstGlance]. <br>	+	<table><tr><td colspan='2'>[[5vlr]] 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=5VLR OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=5VLR FirstGlance]. <br>
-	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=9EM:4-acetyl-1-(3-{4-amino-5-[1-(2,2,2-trifluoroethyl)-1H-pyrazol-5-yl]pyrrolo[2,1-f][1,2,4]triazin-7-yl}phenyl)-3,3-dimethylpiperazin-2-one'>9EM</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]] 2.8Å</td></tr>
-	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PIK3CD ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), PIK3R1, GRB1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>	+	<tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=9EM:4-acetyl-1-(3-{4-amino-5-[1-(2,2,2-trifluoroethyl)-1H-pyrazol-5-yl]pyrrolo[2,1-f][1,2,4]triazin-7-yl}phenyl)-3,3-dimethylpiperazin-2-one'>9EM</scene></td></tr>
-	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Phosphatidylinositol-4,5-bisphosphate_3-kinase Phosphatidylinositol-4,5-bisphosphate 3-kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.153 2.7.1.153] </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=5vlr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5vlr OCA], [https://pdbe.org/5vlr PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=5vlr RCSB], [https://www.ebi.ac.uk/pdbsum/5vlr PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=5vlr ProSAT]</span></td></tr>
-	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[~~http~~://~~oca~~.~~weizmann.ac.il/oca-docs~~/fgij/fg.htm?mol=5vlr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5vlr OCA], [~~http~~://pdbe.org/5vlr PDBe], [~~http~~://www.rcsb.org/pdb/explore.do?structureId=5vlr RCSB], [~~http~~://www.ebi.ac.uk/pdbsum/5vlr PDBsum], [~~http~~://prosat.h-its.org/prosat/prosatexe?pdbcode=5vlr ProSAT]</span></td></tr>	+
	</table>		</table>
	== Disease ==		== Disease ==
-	[~~[http~~://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN]] Activated PIK3-delta syndrome. The disease is caused by mutations affecting the gene represented in this entry.	+	[https://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN] Activated PIK3-delta syndrome. The disease is caused by mutations affecting the gene represented in this entry.
	== Function ==		== Function ==
-	[~~[http~~://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN]] Phosphoinositide-3-kinase (PI3K) that phosphorylates PftdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Mediates immune responses. Plays a role in B-cell development, proliferation, migration, and function. Required for B-cell receptor (BCR) signaling. Mediates B-cell proliferation response to anti-IgM, anti-CD40 and IL4 stimulation. Promotes cytokine production in response to TLR4 and TLR9. Required for antibody class switch mediated by TLR9. Involved in the antigen presentation function of B-cells. Involved in B-cell chemotaxis in response to CXCL13 and sphingosine 1-phosphate (S1P). Required for proliferation, signaling and cytokine production of naive, effector and memory T-cells. Required for T-cell receptor (TCR) signaling. Mediates TCR signaling events at the immune synapse. Activation by TCR leads to antigen-dependent memory T-cell migration and retention to antigenic tissues. Together with PIK3CG participates in T-cell development. Contributes to T-helper cell expansion and differentiation. Required for T-cell migration mediated by homing receptors SELL/CD62L, CCR7 and S1PR1 and antigen dependent recruitment of T-cells. Together with PIK3CG is involved in natural killer (NK) cell development and migration towards the sites of inflammation. Participates in NK cell receptor activation. Have a role in NK cell maturation and cytokine production. Together with PIK3CG is involved in neutrophil chemotaxis and extravasation. Together with PIK3CG participates in neutrophil respiratory burst. Have important roles in mast-cell development and mast cell mediated allergic response. Involved in stem cell factor (SCF)-mediated proliferation, adhesion and migration. Required for allergen-IgE-induced degranulation and cytokine release. The lipid kinase activity is required for its biological function. Isoform 2 may be involved in stabilizing total RAS levels, resulting in increased ERK phosphorylation and increased PI3K activity.<ref>PMID:20081091</ref> <ref>PMID:22020336</ref> [[http://www.uniprot.org/uniprot/P85A_HUMAN P85A_HUMAN]] Binds to activated (phosphorylated) protein-Tyr kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Plays an important role in signaling in response to FGFR1, FGFR2, FGFR3, FGFR4, KITLG/SCF, KIT, PDGFRA and PDGFRB. Likewise, plays a role in ITGB2 signaling.<ref>PMID:7518429</ref> <ref>PMID:17626883</ref> <ref>PMID:19805105</ref>	+	[https://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN] Phosphoinositide-3-kinase (PI3K) that phosphorylates PftdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Mediates immune responses. Plays a role in B-cell development, proliferation, migration, and function. Required for B-cell receptor (BCR) signaling. Mediates B-cell proliferation response to anti-IgM, anti-CD40 and IL4 stimulation. Promotes cytokine production in response to TLR4 and TLR9. Required for antibody class switch mediated by TLR9. Involved in the antigen presentation function of B-cells. Involved in B-cell chemotaxis in response to CXCL13 and sphingosine 1-phosphate (S1P). Required for proliferation, signaling and cytokine production of naive, effector and memory T-cells. Required for T-cell receptor (TCR) signaling. Mediates TCR signaling events at the immune synapse. Activation by TCR leads to antigen-dependent memory T-cell migration and retention to antigenic tissues. Together with PIK3CG participates in T-cell development. Contributes to T-helper cell expansion and differentiation. Required for T-cell migration mediated by homing receptors SELL/CD62L, CCR7 and S1PR1 and antigen dependent recruitment of T-cells. Together with PIK3CG is involved in natural killer (NK) cell development and migration towards the sites of inflammation. Participates in NK cell receptor activation. Have a role in NK cell maturation and cytokine production. Together with PIK3CG is involved in neutrophil chemotaxis and extravasation. Together with PIK3CG participates in neutrophil respiratory burst. Have important roles in mast-cell development and mast cell mediated allergic response. Involved in stem cell factor (SCF)-mediated proliferation, adhesion and migration. Required for allergen-IgE-induced degranulation and cytokine release. The lipid kinase activity is required for its biological function. Isoform 2 may be involved in stabilizing total RAS levels, resulting in increased ERK phosphorylation and increased PI3K activity.<ref>PMID:20081091</ref> <ref>PMID:22020336</ref>
-	~~<div style="background-color:#fffaf0;">~~	+
-	~~== Publication Abstract from PubMed ==~~	+
-	PI3Kdelta plays an important role controlling immune cell function and has therefore been identified as a potential target for the treatment of immunological disorders. This article highlights our work toward the identification of a potent, selective, and efficacious PI3Kdelta inhibitor. Through careful SAR, the successful replacement of a polar pyrazole group by a simple chloro or trifluoromethyl group led to improved Caco-2 permeability, reduced Caco-2 efflux, reduced hERG PC activity, and increased selectivity profile while maintaining potency in the CD69 hWB assay. The optimization of the aryl substitution then identified a 4'-CN group that improved the human/rodent correlation in microsomal metabolic stability. Our lead molecule is very potent in PK/PD assays and highly efficacious in a mouse collagen-induced arthritis model.	+
-		+
-	Identification of a Potent, Selective, and Efficacious Phosphatidylinositol 3-Kinase delta (PI3Kdelta) Inhibitor for the Treatment of Immunological Disorders.,Liu Q, Shi Q, Marcoux D, Batt DG, Cornelius L, Qin LY, Ruan Z, Neels J, Beaudoin-Bertrand M, Srivastava AS, Li L, Cherney RJ, Gong H, Watterson SH, Weigelt C, Gillooly KM, McIntyre KW, Xie JH, Obermeier MT, Fura A, Sleczka B, Stefanski K, Fancher RM, Padmanabhan S, Rp T, Kundu I, Rajareddy K, Smith R, Hennan JK, Xing D, Fan J, Levesque PC, Ruan Q, Pitt S, Zhang R, Pedicord D, Pan J, Yarde M, Lu H, Lippy J, Goldstine C, Skala S, Rampulla RA, Mathur A, Gupta A, Arunachalam PN, Sack JS, Muckelbauer JK, Cvijic ME, Salter-Cid LM, Bhide RS, Poss MA, Hynes J, Carter PH, Macor JE, Ruepp S, Schieven GL, Tino JA J Med Chem. 2017 Jun 22;60(12):5193-5208. doi: 10.1021/acs.jmedchem.7b00618. Epub, 2017 Jun 5. PMID:28541707<ref>PMID:28541707</ref>	+
-		+
-	~~From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>~~	+
-	~~</div>~~	+
-	~~<div class="pdbe-citations 5vlr" style="background-color:#fffaf0;"></div~~>	+
	== References ==		== References ==
	<references/>		<references/>
	__TOC__		__TOC__
	</StructureSection>		</StructureSection>
-	[[Category: ~~Human~~]]	+	[[Category: Homo sapiens]]
-	[[Category: ~~Phosphatidylinositol-4,5-bisphosphate 3-kinase~~]]	+	[[Category: Large Structures]]
-	[[Category: Sack~~, J S]]~~	+	[[Category: Sack JS]]
-	~~[[Category: Inhibitor]]~~	+
-	~~[[Category: Lipid kinase]]~~	+
-	~~[[Category: Pi3k delta]]~~	+
-	~~[[Category: Transferase-transferase inhibitor complex]]~~	+
-	~~[[Category: Transferase-transferase regulator complex~~]]	+

OCA at 08:21, 16 November 2017

OCA — Thu, 16 Nov 2017 08:21:40 GMT

←Older revision		Revision as of 08:21, 16 November 2017
Line 1:		Line 1:
-	'''Unreleased structure'''

-	The entry ~~5vlr~~ is ~~ON HOLD~~ ~~until Paper~~ Publication	+	==CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR==
		+	<StructureSection load='5vlr' size='340' side='right' caption='[[5vlr]], [[Resolution\|resolution]] 2.80Å' scene=''>
		+	== Structural highlights ==
		+	<table><tr><td colspan='2'>[[5vlr]] is a 2 chain structure with sequence from [http://en.wikipedia.org/wiki/Human Human]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=5VLR OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5VLR FirstGlance]. <br>
		+	</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand\|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=9EM:4-acetyl-1-(3-{4-amino-5-[1-(2,2,2-trifluoroethyl)-1H-pyrazol-5-yl]pyrrolo[2,1-f][1,2,4]triazin-7-yl}phenyl)-3,3-dimethylpiperazin-2-one'>9EM</scene></td></tr>
		+	<tr id='gene'><td class="sblockLbl"><b>[[Gene\|Gene:]]</b></td><td class="sblockDat">PIK3CD ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN]), PIK3R1, GRB1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=9606 HUMAN])</td></tr>
		+	<tr id='activity'><td class="sblockLbl"><b>Activity:</b></td><td class="sblockDat"><span class='plainlinks'>[http://en.wikipedia.org/wiki/Phosphatidylinositol-4,5-bisphosphate_3-kinase Phosphatidylinositol-4,5-bisphosphate 3-kinase], with EC number [http://www.brenda-enzymes.info/php/result_flat.php4?ecno=2.7.1.153 2.7.1.153] </span></td></tr>
		+	<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=5vlr FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=5vlr OCA], [http://pdbe.org/5vlr PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=5vlr RCSB], [http://www.ebi.ac.uk/pdbsum/5vlr PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=5vlr ProSAT]</span></td></tr>
		+	</table>
		+	== Disease ==
		+	[[http://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN]] Activated PIK3-delta syndrome. The disease is caused by mutations affecting the gene represented in this entry.
		+	== Function ==
		+	[[http://www.uniprot.org/uniprot/PK3CD_HUMAN PK3CD_HUMAN]] Phosphoinositide-3-kinase (PI3K) that phosphorylates PftdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Mediates immune responses. Plays a role in B-cell development, proliferation, migration, and function. Required for B-cell receptor (BCR) signaling. Mediates B-cell proliferation response to anti-IgM, anti-CD40 and IL4 stimulation. Promotes cytokine production in response to TLR4 and TLR9. Required for antibody class switch mediated by TLR9. Involved in the antigen presentation function of B-cells. Involved in B-cell chemotaxis in response to CXCL13 and sphingosine 1-phosphate (S1P). Required for proliferation, signaling and cytokine production of naive, effector and memory T-cells. Required for T-cell receptor (TCR) signaling. Mediates TCR signaling events at the immune synapse. Activation by TCR leads to antigen-dependent memory T-cell migration and retention to antigenic tissues. Together with PIK3CG participates in T-cell development. Contributes to T-helper cell expansion and differentiation. Required for T-cell migration mediated by homing receptors SELL/CD62L, CCR7 and S1PR1 and antigen dependent recruitment of T-cells. Together with PIK3CG is involved in natural killer (NK) cell development and migration towards the sites of inflammation. Participates in NK cell receptor activation. Have a role in NK cell maturation and cytokine production. Together with PIK3CG is involved in neutrophil chemotaxis and extravasation. Together with PIK3CG participates in neutrophil respiratory burst. Have important roles in mast-cell development and mast cell mediated allergic response. Involved in stem cell factor (SCF)-mediated proliferation, adhesion and migration. Required for allergen-IgE-induced degranulation and cytokine release. The lipid kinase activity is required for its biological function. Isoform 2 may be involved in stabilizing total RAS levels, resulting in increased ERK phosphorylation and increased PI3K activity.<ref>PMID:20081091</ref> <ref>PMID:22020336</ref> [[http://www.uniprot.org/uniprot/P85A_HUMAN P85A_HUMAN]] Binds to activated (phosphorylated) protein-Tyr kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Plays an important role in signaling in response to FGFR1, FGFR2, FGFR3, FGFR4, KITLG/SCF, KIT, PDGFRA and PDGFRB. Likewise, plays a role in ITGB2 signaling.<ref>PMID:7518429</ref> <ref>PMID:17626883</ref> <ref>PMID:19805105</ref>
		+	<div style="background-color:#fffaf0;">
		+	== Publication Abstract from PubMed ==
		+	PI3Kdelta plays an important role controlling immune cell function and has therefore been identified as a potential target for the treatment of immunological disorders. This article highlights our work toward the identification of a potent, selective, and efficacious PI3Kdelta inhibitor. Through careful SAR, the successful replacement of a polar pyrazole group by a simple chloro or trifluoromethyl group led to improved Caco-2 permeability, reduced Caco-2 efflux, reduced hERG PC activity, and increased selectivity profile while maintaining potency in the CD69 hWB assay. The optimization of the aryl substitution then identified a 4'-CN group that improved the human/rodent correlation in microsomal metabolic stability. Our lead molecule is very potent in PK/PD assays and highly efficacious in a mouse collagen-induced arthritis model.

-	~~Authors:~~ Sack, J.S.	+	Identification of a Potent, Selective, and Efficacious Phosphatidylinositol 3-Kinase delta (PI3Kdelta) Inhibitor for the Treatment of Immunological Disorders.,Liu Q, Shi Q, Marcoux D, Batt DG, Cornelius L, Qin LY, Ruan Z, Neels J, Beaudoin-Bertrand M, Srivastava AS, Li L, Cherney RJ, Gong H, Watterson SH, Weigelt C, Gillooly KM, McIntyre KW, Xie JH, Obermeier MT, Fura A, Sleczka B, Stefanski K, Fancher RM, Padmanabhan S, Rp T, Kundu I, Rajareddy K, Smith R, Hennan JK, Xing D, Fan J, Levesque PC, Ruan Q, Pitt S, Zhang R, Pedicord D, Pan J, Yarde M, Lu H, Lippy J, Goldstine C, Skala S, Rampulla RA, Mathur A, Gupta A, Arunachalam PN, Sack JS, Muckelbauer JK, Cvijic ME, Salter-Cid LM, Bhide RS, Poss MA, Hynes J, Carter PH, Macor JE, Ruepp S, Schieven GL, Tino JA J Med Chem. 2017 Jun 22;60(12):5193-5208. doi: 10.1021/acs.jmedchem.7b00618. Epub, 2017 Jun 5. PMID:28541707<ref>PMID:28541707</ref>

-	~~Description: CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO~~-~~ETHYL~~-~~PYRAZOL-PYROLOTRIAZINE INHIBITOR~~	+	From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br>
-	[[Category: ~~Unreleased Structures~~]]	+	</div>
-	[[Category: Sack, J.S]]	+	<div class="pdbe-citations 5vlr" style="background-color:#fffaf0;"></div>
		+	== References ==
		+	<references/>
		+	__TOC__
		+	</StructureSection>
		+	[[Category: Human]]
		+	[[Category: Phosphatidylinositol-4,5-bisphosphate 3-kinase]]
		+	[[Category: Sack, J S]]
		+	[[Category: Inhibitor]]
		+	[[Category: Lipid kinase]]
		+	[[Category: Pi3k delta]]
		+	[[Category: Transferase-transferase inhibitor complex]]
		+	[[Category: Transferase-transferase regulator complex]]

OCA at 11:10, 10 May 2017

OCA — Wed, 10 May 2017 11:10:11 GMT

←Older revision		Revision as of 11:10, 10 May 2017
Line 1:		Line 1:
	'''Unreleased structure'''		'''Unreleased structure'''

-	The entry 5vlr is ON HOLD	+	The entry 5vlr is ON HOLD until Paper Publication

	Authors: Sack, J.S.		Authors: Sack, J.S.

OCA: Protected "5vlr" [edit=sysop:move=sysop]

OCA — Thu, 04 May 2017 11:27:30 GMT

Protected "5vlr" [edit=sysop:move=sysop]

←Older revision

Revision as of 11:27, 4 May 2017

OCA: New page: '''Unreleased structure''' The entry 5vlr is ON HOLD Authors: Sack, J.S. Description: CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR...

OCA — Thu, 04 May 2017 11:27:28 GMT

New page: '''Unreleased structure''' The entry 5vlr is ON HOLD Authors: Sack, J.S. Description: CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR...

New page

'''Unreleased structure'''

The entry 5vlr is ON HOLD

Authors: Sack, J.S.

Description: CRYSTAL STRUCTURE OF PI3K DELTA IN COMPLEX WITH A TRIFLUORO-ETHYL-PYRAZOL-PYROLOTRIAZINE INHIBITOR
[[Category: Unreleased Structures]]
[[Category: Sack, J.S]]