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- W2035154619 endingPage "1383" @default.
- W2035154619 startingPage "1371" @default.
- W2035154619 abstract "Introduction: Formation of blood vessels from pre-existing ones, also termed angiogenesis, is of crucial importance for the outgrowth of tumours beyond 1 – 2 mm3. Therefore, anti-angiogenic therapies, mainly focussing on inhibition of vascular endothelial growth factor (VEGF) are used in clinical therapy. However, although initially reducing tumour size, therapy resistance occurs frequently and new targets are needed. A possible target is activin receptor-like kinase (ALK)-1, a transforming growth factor (TGF)-β type-I receptor, which binds bone morphogenetic protein (BMP)-9 and -10 with high affinity and has an important role in regulating angiogenesis. Areas covered: Several approaches to interfere with ALK1 signalling have been developed, that is, ALK1 neutralising antibodies and a soluble ALK1 extracellular domain/Fc fusion protein (ALK1-Fc), acting as a ligand trap. In this review, we discuss the involvement of ALK1 in angiogenesis, in a variety of diseases and the current status of the development of ALK1 inhibitors for cancer therapy. Expert opinion: Based on current, mainly preclinical studies on inhibition of ALK1 signalling by ligand traps and neutralising antibodies, targeting ALK1 seems very promising. Both ALK1-Fc and neutralising antibodies strongly inhibit angiogenesis in vitro and in vivo. The results from the first Phase I clinical trials are to be reported soon and multiple Phase II studies are ongoing." @default.
- W2035154619 created "2016-06-24" @default.
- W2035154619 creator A5026440752 @default.
- W2035154619 creator A5046914597 @default.
- W2035154619 creator A5060111407 @default.
- W2035154619 date "2013-09-21" @default.
- W2035154619 modified "2023-10-16" @default.
- W2035154619 title "Activin receptor-like kinase 1 as a target for anti-angiogenesis therapy" @default.
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- W2035154619 doi "https://doi.org/10.1517/13543784.2013.837884" @default.
- W2035154619 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24053899" @default.
- W2035154619 hasPublicationYear "2013" @default.
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