	US 12,448,424 B2
	Compositions and methods relating to the treatment of diseases
William Stimson, Glasgow (GB)
Assigned to ILC Therapeutics, LTD, Lanarkshire (GB)
Filed by ILC Therapeutics, LTD, Lanarkshire (GB)
Filed on Jan. 25, 2022, as Appl. No. 17/583,971.
Application 17/583,971 is a continuation of application No. 15/760,200, granted, now 11,267,860, previously published as PCT/GB2016/052841, filed on Sep. 14, 2016.
Claims priority of application No. 1516303 (GB), filed on Sep. 15, 2015; and application No. 1516437 (GB), filed on Sep. 16, 2015.
Prior Publication US 2022/0220183 A1, Jul. 14, 2022
Int. Cl. C07K 14/56 (2006.01); A61K 38/21 (2006.01); A61K 39/00 (2006.01); A61K 39/35 (2006.01); C07K 19/00 (2006.01)

CPC C07K 14/56 (2013.01) [A61K 38/212 (2013.01); A61K 39/0011 (2013.01); A61K 39/35 (2013.01); C07K 19/00 (2013.01); C07K 2319/00 (2013.01)]

8 Claims

1. A hybrid IFN-α comprising the amino acid sequence of SEQ ID NO:3 having one or more of the following amino acid substitutions: a Glu to Lys mutation at position 71 of SEQ ID NO:3, a Glu to Asp mutation at position 78 of SEQ ID NO:3, a Gln to Glu mutation at position 79 of SEQ ID NO:3, a Ser to Tyr mutation at position 86 of SEQ ID NO:3, and an Arg to Lys mutation at position 121 of SEQ ID NO:3,

wherein the hybrid IFN-α comprises a primary interferon receptor binding site of IFN-α10 and a primary interferon receptor binding site of IFN-α14, and

wherein the hybrid IFN-α has increased affinity for interferon receptor 1 (IFNR1) and interferon receptor 2 (IFNR2) compared to unmodified IFN-α10 and unmodified IFN-α14, and

wherein the hybrid IFN-α enhances a Th1-mediated immune response and suppresses a Th2/Th17-mediated immune response.