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A role for TREX components in the release of spliced mRNA from nuclear speckle domains

Nature communications, 2010-10, Vol.1 (7), p.97-97, Article 97

2010

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Human mRNA Export Machinery Recruited to the 5′ End of mRNA

Cell, 2006-12, Vol.127 (7), p.1389-1400

2006

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ATP is required for interactions between UAP56 and two conserved mRNA export proteins, Aly and CIP29, to assemble the TREX complex

Genes & development, 2010-09, Vol.24 (18), p.2043-2053

2010

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GBT440 reverses sickling of sickled red blood cells under hypoxic conditions in vitro

Hematology reports, 2018-05, Vol.10 (2), p.7419-7419

2018

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Discovery of GBT440, an Orally Bioavailable R‑State Stabilizer of Sickle Cell Hemoglobin

ACS medicinal chemistry letters, 2017-03, Vol.8 (3), p.321-326

2017

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The proteins PDIP3 and ZC11A associate with the human TREX complex in an ATP-dependent manner and function in mRNA export

PloS one, 2012-08, Vol.7 (8), p.e43804-e43804

2012

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Functional coupling of RNAP II transcription to spliceosome assembly

Genes & development, 2006-05, Vol.20 (9), p.1100-1109

2006

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GBT440 Inhibits Sickling of Sickle Cell Trait Blood Under In Vitro Conditions Mimicking Strenuous Exercise

Hematology reports, 2016-09, Vol.8 (3), p.6637-6637

2016

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The effect of the antisickling compound GBT1118 on the permeability of red blood cells from patients with sickle cell anemia

Physiological reports, 2019-03, Vol.7 (6), p.e14027-n/a

2019

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GBT440 improves red blood cell deformability and reduces viscosity of sickle cell blood under deoxygenated conditions

Clinical hemorheology and microcirculation, 2018-01, Vol.70 (1), p.95-105

2018

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Increased Hemoglobin Affinity for Oxygen with GBT021601 Reduces Pulmonary Hypertension and Lung Vascular Inflammation in a Murine Model of Sickle Cell Disease

Blood, 2022-11, Vol.140 (Supplement 1), p.5375-5376

2022

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GBT021601 Prevents Microvascular Dysfunction and Improves Hypoxia-Reoxygenation-Induced Vaso-Occlusion in a Murine Model of Sickle Cell Disease

Blood, 2022-11, Vol.140 (Supplement 1), p.5377-5378

2022

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GBT440 increases haemoglobin oxygen affinity, reduces sickling and prolongs RBC half‐life in a murine model of sickle cell disease

British journal of haematology, 2016-10, Vol.175 (1), p.141-153

2016

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A phase 1/2 ascending dose study and open-label extension study of voxelotor in patients with sickle cell disease

Blood, 2019-04, Vol.133 (17), p.1865-1875

2019

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GBT021601 Increases Hemoglobin and Improves Red Blood Cell Deformability without Rebound Hyperviscosity upon Drug Clearance in a Sickle Mouse Model

Blood, 2022-11, Vol.140 (Supplement 1), p.5393-5394

2022

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Predictive Biomarker Analysis from the GBT021601 Survival Study in Townes Sickle Mice

Blood, 2023-11, Vol.142 (Supplement 1), p.14-14

2023

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Pharmacodynamic Results from Phase 1 Studies of GBT021601, a Next-Generation HbS Polymerization Inhibitor for Treatment of Sickle Cell Disease

Blood, 2022-11, Vol.140 (Supplement 1), p.24-25

2022

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Evaluation of GBT021601 As a Therapeutic Agent to Restore Bone Marrow Health and Effective Erythropoiesis in a Sickle Mouse Model

Blood, 2023-11, Vol.142 (Supplement 1), p.16-16

2023

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GBT021601 Inhibits HbS Polymerization, Prevents RBC Sickling and Improves the Pathophysiology of Sickle Cell Disease in a Murine Model

Blood, 2020-11, Vol.136 (Supplement 1), p.7-8

2020

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Increased hemoglobin affinity for oxygen with GBT1118 improves hypoxia tolerance in sickle cell mice

American journal of physiology. Heart and circulatory physiology, 2021-08, Vol.321 (2), p.H400-H411

2021

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Pharmacological Increase of Hb-O2 Affinity with a Voxelotor Analog Does Not Decrease Brain Tissue pO2 or Limit O2 Extraction in Brain Tissues of Sickle Cell Mice

Blood, 2019-11, Vol.134 (Supplement_1), p.3564-3564

2019

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GBT021601 improves red blood cell health and the pathophysiology of sickle cell disease in a murine model

British journal of haematology, 2023-07, Vol.202 (1), p.173-183

2023

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GBT1118, a potent allosteric modifier of hemoglobin O 2 affinity, increases tolerance to severe hypoxia in mice

American journal of physiology. Heart and circulatory physiology, 2017-08, Vol.313 (2), p.H381-H391

2017

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GBT1118, a potent allosteric modifier of hemoglobin O2 affinity, increases tolerance to severe hypoxia in mice

American journal of physiology. Heart and circulatory physiology, 2017-08, Vol.313 (2), p.H381-H391

2017

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Effects of an allosteric hemoglobin affinity modulator on arterial blood gases and cardiopulmonary responses during normoxic and hypoxic low-intensity exercise

Journal of applied physiology (1985), 2020-06, Vol.128 (6), p.1467-1476

2020

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A role for TREX components in the release of spliced mRNA from nuclear speckle domains

Human mRNA Export Machinery Recruited to the 5′ End of mRNA

ATP is required for interactions between UAP56 and two conserved mRNA export proteins, Aly and CIP29, to assemble the TREX complex

GBT440 reverses sickling of sickled red blood cells under hypoxic conditions in vitro

Discovery of GBT440, an Orally Bioavailable R‑State Stabilizer of Sickle Cell Hemoglobin

The proteins PDIP3 and ZC11A associate with the human TREX complex in an ATP-dependent manner and function in mRNA export

Functional coupling of RNAP II transcription to spliceosome assembly

GBT440 Inhibits Sickling of Sickle Cell Trait Blood Under In Vitro Conditions Mimicking Strenuous Exercise

The effect of the antisickling compound GBT1118 on the permeability of red blood cells from patients with sickle cell anemia

GBT440 improves red blood cell deformability and reduces viscosity of sickle cell blood under deoxygenated conditions

Increased Hemoglobin Affinity for Oxygen with GBT021601 Reduces Pulmonary Hypertension and Lung Vascular Inflammation in a Murine Model of Sickle Cell Disease

GBT021601 Prevents Microvascular Dysfunction and Improves Hypoxia-Reoxygenation-Induced Vaso-Occlusion in a Murine Model of Sickle Cell Disease

GBT440 increases haemoglobin oxygen affinity, reduces sickling and prolongs RBC half‐life in a murine model of sickle cell disease

A phase 1/2 ascending dose study and open-label extension study of voxelotor in patients with sickle cell disease

GBT021601 Increases Hemoglobin and Improves Red Blood Cell Deformability without Rebound Hyperviscosity upon Drug Clearance in a Sickle Mouse Model

Predictive Biomarker Analysis from the GBT021601 Survival Study in Townes Sickle Mice

Pharmacodynamic Results from Phase 1 Studies of GBT021601, a Next-Generation HbS Polymerization Inhibitor for Treatment of Sickle Cell Disease

Evaluation of GBT021601 As a Therapeutic Agent to Restore Bone Marrow Health and Effective Erythropoiesis in a Sickle Mouse Model

GBT021601 Inhibits HbS Polymerization, Prevents RBC Sickling and Improves the Pathophysiology of Sickle Cell Disease in a Murine Model

Increased hemoglobin affinity for oxygen with GBT1118 improves hypoxia tolerance in sickle cell mice

Pharmacological Increase of Hb-O2 Affinity with a Voxelotor Analog Does Not Decrease Brain Tissue pO2 or Limit O2 Extraction in Brain Tissues of Sickle Cell Mice

GBT021601 improves red blood cell health and the pathophysiology of sickle cell disease in a murine model

GBT1118, a potent allosteric modifier of hemoglobin O 2 affinity, increases tolerance to severe hypoxia in mice

GBT1118, a potent allosteric modifier of hemoglobin O2 affinity, increases tolerance to severe hypoxia in mice

Effects of an allosteric hemoglobin affinity modulator on arterial blood gases and cardiopulmonary responses during normoxic and hypoxic low-intensity exercise

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