A clinical update on BLU-782, an investigational selective ALK2 inhibitor in development for fibrodysplasia ossificans progressiva (FOP)

被引：0

作者：

Davis, Alison ^{[1
]}

Albayya, Faris ^{[1
]}

Lobbardi, Riadh ^{[1
]}

Palmer, Michael ^{[1
]}

Sherwin, Cori Ann ^{[1
]}

Green, Sara ^{[1
]}

Stevison, Faith ^{[1
]}

Kim, Sean ^{[1
]}

Wilkie, Gordon ^{[1
]}

Kadambi, Vivek ^{[1
]}

Dorsch, Marion ^{[1
]}

Boral, Andy ^{[1
]}

LaBranche, Timothy ^{[1
]}

Hurtt, Mark ^{[2
]}

Schwabb, Robert ^{[3
]}

Stewart, Rachel ^{[4
]}

Lyon, Morgan ^{[4
]}

Pauplis, Rachel ^{[4
]}

机构：

[1] Blueprint Med, Cambridge, MA USA

[2] Hurtt Consulting, Groton, CT USA

[3] Celerion, Lincoln, NE USA

[4] Invicro, Boston, MA USA

来源：

JOURNAL OF BONE AND MINERAL RESEARCH | 2019年 / 34卷

关键词：

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

LB SUN-108

引用

页码：290 / 290

页数：1

共 35 条

[31] Mutant ALK2 receptors found in patients with typical and variant fibrodysplasia ossificans progressiva are activated by different BMP type II receptors through phosphorylation at Thr203
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[32] Disease-causing allele-specific silencing against the ALK2 mutants, R206H and G356D, in fibrodysplasia ossificans progressiva
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[33] Disease-causing allele-specific silencing against the ALK2 mutants, R206H and G356D, in fibrodysplasia ossificans progressiva
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[35] A novel mutation of ALK2, L196P, found in the most benign case of fibrodysplasia ossificans progressiva activates BMP-specific intracellular signaling equivalent to a typical mutation, R206H
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