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Biological and Environmental Research Ontology
| Id | http://purl.obolibrary.org/obo/NCIT_C148455
http://purl.obolibrary.org/obo/NCIT_C148455
|
|---|---|
| Preferred Name | Emavusertib |
| Definitions |
An orally bioavailable, reversible inhibitor of interleukin-1 receptor-associated kinase 4 (IRAK4), with potential antineoplastic, immunomodulating and anti-inflammatory activities. Upon oral administration, emavusertib targets, binds to, and blocks the kinase activity of IRAK4. This inhibits IRAK4-mediated signaling, prevents the activation of IRAK4-mediated nuclear factor-kappa B (NF-kB) signaling and decreases the expression of inflammatory cytokines and certain pro-survival factors. This inhibits proliferation of IRAK4-overactivated tumor cells, which are found in cells harboring MYD88 activating mutations or those with overactivated toll-like receptor (TLR) pathways. In addition, CA-4948 may inhibit inflammation and immune-mediated cell destruction in inflammatory and auto-immune diseases where TLR or interleukin 1 receptor (IL-1R) signaling is overactivated and MYD88 is dysregulated. IRAK4, a serine/threonine-protein kinase that plays a key role in both the TLR and IL-1R signaling pathways, is activated though the adaptor protein MYD88 and links the TLR and IL-1R signaling pathway to the NF-kB pathway.
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| Type | http://www.w3.org/2002/07/owl#Class |
All Properties
| definition | An orally bioavailable, reversible inhibitor of interleukin-1 receptor-associated kinase 4 (IRAK4), with potential antineoplastic, immunomodulating and anti-inflammatory activities. Upon oral administration, emavusertib targets, binds to, and blocks the kinase activity of IRAK4. This inhibits IRAK4-mediated signaling, prevents the activation of IRAK4-mediated nuclear factor-kappa B (NF-kB) signaling and decreases the expression of inflammatory cytokines and certain pro-survival factors. This inhibits proliferation of IRAK4-overactivated tumor cells, which are found in cells harboring MYD88 activating mutations or those with overactivated toll-like receptor (TLR) pathways. In addition, CA-4948 may inhibit inflammation and immune-mediated cell destruction in inflammatory and auto-immune diseases where TLR or interleukin 1 receptor (IL-1R) signaling is overactivated and MYD88 is dysregulated. IRAK4, a serine/threonine-protein kinase that plays a key role in both the TLR and IL-1R signaling pathways, is activated though the adaptor protein MYD88 and links the TLR and IL-1R signaling pathway to the NF-kB pathway. |
|---|---|
| prefLabel | Emavusertib
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| label | Emavusertib
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| NCI_META_CUI | CL551081
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| PDQ_Closed_Trial_Search_ID | 794871
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| code | C148455
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| Has_Target | |
| prefixIRI | NCIT:C148455
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| in_subset |
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| Display_Name | Emavusertib
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| Preferred_Name | Emavusertib
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| FDA_UNII_Code | MH5DMF9JKY
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| Contributing_Source |
CTRP
FDA
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| Maps_To | IRAK4 Inhibitor CA-4948
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| CAS_Registry | 1801343-74-7
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| NCI_Drug_Dictionary_ID | 794871
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| type | |
| Is_Value_For_GDC_Property | |
| subClassOf | |
| PDQ_Open_Trial_Search_ID | 794871
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| Semantic_Type | Pharmacologic Substance
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