IP Library Granted Patent US 12,448,424
Granted Patent B2
US 12,448,424 · App. 17/583,971 · Granted Oct 21, 2025

Compositions and methods relating to the treatment of diseases

Inventor: William Stimson (Glasgow, GB)
Assignee: ILC Therapeutics, LTD
C07K14/56A61K38/212A61K39/0011A61K39/35C07K19/00C07K2319/00
View Patent ↗
Loading inventors, assignments & file history…
Monitor This Case
Get email alerts when status or documents change.
Order Certified Copies
Most orders are placed with the USPTO same day — all within 24 business hours.
Order via The Patent Place →
Pre-filled with this patent's details
Quick Facts
Patent No.
US 12,448,424
App. No.
17/583,971
Granted
Oct 21, 2025
Kind
B2
Abstract

The present invention relates to compositions and methods for promoting the induction of a cell-mediated immune response (such as that mediated by Th1 cells) and the suppression of a humoral or allergic immune response (such as that mediated by Th2 and Th17 cells). In particular, the invention relates to compositions and methods for preventing or treating allergy, such as food allergy, and associated allergic diseases, and conditions where an exaggerated Th17 response plays a detrimental role, such as inflammatory responses and autoimmune diseases. The invention further extends to the use of the compositions of the invention in the treatment and/or prophylaxis of allergy and associated allergic diseases and also of cancer.

Claims (11)

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.

2. The hybrid IFN-α of claim 1 , wherein the hybrid IFN-α comprises the amino acid sequence of SEQ ID NO: 1.

3. A pharmaceutical composition comprising the hybrid IFN-α of claim 1 .

4. The pharmaceutical composition of claim 3 , wherein the hybrid IFN-α is formulated for administration to a subject in combination with a vaccine composition.

5. The pharmaceutical composition of claim 4 , wherein the vaccine composition comprises at least one allergen or antigen capable of mediating a Th2/Th17 immune response.

6. The pharmaceutical composition of claim 5 , wherein the at least one allergen or antigen comprises a food allergen, a tumour antigen, a tumour-specific antigen, or a tumour-associated antigen.

7. The pharmaceutical composition of claim 3 , wherein the hybrid IFN-α is formulated for oral administration.

8. The pharmaceutical composition of claim 3 , wherein the pharmaceutical composition further comprises a pharmaceutically acceptable excipient, diluent, or carrier.

Assignments (2)
CHANGE OF NAME Recorded Aug 13, 2022
From: ALFACYTE LTD
To: ILC THERAPEUTICS LTD
Reel/Frame 061165/0586 →
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Jul 29, 2022
From: STIMSON, WILLIAM
To: ALFACYTE LTD
Reel/Frame 060667/0719 →
Priority Claims (2)
GB 1516303 · Sep 15, 2015 · national
GB 1516437 · Sep 16, 2015 · national
Continuity (2)
Continuation 15760200
Related Publication 20220220183A1 · Jul 14, 2022
References Cited (31)
US 6350589B1 · Morris et al. · 2002 [cited by applicant]
WO WO199524212A1 · 1995 [cited by applicant]
WO WO2007044083A1 · 2007 [cited by applicant]
WO WO2008041014A1 · 2008 [cited by applicant]
WO WO2014037717A1 · 2014 [cited by applicant]
WO WO2014151422A1 · 2014 [cited by applicant]
WO WO2015136287A2 · 2015 [cited by applicant]
Bork. Powers and Pitfalls in Sequence Analysis: The 70% Hurdle. Genome Research, 2000, 10:398-400 (Year: 2000). [cited by examiner]
Greenspan et al. 1999. Defining epitopes: It's not as easy as it seems; Nature Biotechnology, 17:936-937 (Year: 1999). [cited by examiner]
Bowie et al. Deciphering the Message in Protein Sequences: Tolerance to Amino Acid Substitutions. Science, 1990, 247:1306-1310 (Year: 1990). [cited by examiner]
Burgess et al. Possible Dissociation of the Heparin-binding and Mitogenic Activities of Heparin-binding (Acidic Fibroblast) Growth Factor-1 from Its Receptor-binding Activities by Site-directed Mutagenesis of a Single L… [cited by examiner]
Lazar et al. Transforming Growth Factor alpha: Mutation of Aspartic Acid 47 and Leucine 48 Results in Different Biological Activities. Mol. Cell. Biol., 8:1247-1252, 1988 (Year: 1988). [cited by examiner]
CA Application No. 2,998,456, Office Action mailed Jul. 28, 2023. [cited by applicant]
U.S. Appl. No. 15/760,200, filed Mar. 14, 2018, now U.S. Pat. No. 11,267,860, Issued. [cited by applicant]
Bastid et al. “The Emerging Role of the IL-17BIL-17RB Pathway in cancer,” Front. Immunol., 11:718, (Apr. 2020). [cited by applicant]
Crow, M.K., “Interferon-alpha: a therapeutic target in systemic lupus erythematosus,” Rheum. Dis. Clin. North Am., 36(1):173, (2010). [cited by applicant]
Fabregat et al. “TGF-beta signaling in cancer treatment,” Curr Pharm Des., 20(17):2934-47, (May 14, 2014)—abstract. [cited by applicant]
Ge et al. “Biology of Interleukin-17 and Its Pathophysiological Significance in Sepsis,” Frontiers in Immunology, 11:1558, (Jul. 2020). [cited by applicant]
Goldstein, D. et al., “The Role of Interferon in Cancer Therapy: A Current Perspective,” CA Cancer J. Clin., 38:258-277, (1988). [cited by applicant]
Gonzales-Van Horn, S.R. et al., “Interferon at the crossroads of allergy and viral infections,” J. Leuk. Biol., 98:185-194, (2015). [cited by applicant]
Jin et al. “IL-17 cytokines in immunity and inflammation,” Emerg Microbes Infect., 2(9):e60, (Sep. 13, 2013). [cited by applicant]
Katayama “Anti-interleukin-17A and anti-interleukin-23 antibodies may be effective against Alzheimer's disease: Role of neutrophils in the pathogenesis,” Brain Behav., 10(1):e01504, (Jan. 2020). [cited by applicant]
Kim et al. “Multi-cellular natural killer (NK) cell clusters enhance NK cell activation through localizing IL-2 within the cluster,” Scientific Reports, 7:40623, (Jan. 11, 2017). [cited by applicant]
Kotredes, Kevin P. et al., “The Protective Role of Type I Interferons in the Gastrointestinal Tract,” Frontiers in Immunology, 8:410, (2017). [cited by applicant]
Li et al., “Interleukin 17 receptor-based signaling and implications for disease,” Nat. Immunol., 20 (12): 1594-1602, (2019). [cited by applicant]
Mangodt et al., “The role of Th17 and Treg responses in the pathogenesis of RSV infection,” Pediatric Research, 78(5):483-491, (Nov. 2015). [cited by applicant]
Pai et al., “Wnt/beta-catenin pathway: modulating anticancer immune response,” J Hematol Oncol, 10(1):101, (May 5, 2017). [cited by applicant]
Psarras, Antonios et al., “Type I interferon-mediated autoimmune diseases: pathogenesis, diagnosis and targeted therapy,” Rheumatology, 56:1662-1675, (2017). [cited by applicant]
Razi et al. “IL-17 and colorectal cancer: From carcinogenesis to treatment,” Cytokine 116:7-12, (2019)—abstract. [cited by applicant]
Santhanam, S. et al., “Potential of interferon-alpha in solid tumors,” Part 2. Biodrugs, 16(5):349-372, (2002). [cited by applicant]
PCT/GB2016/052841 International Search Report and Written Opinion mailed Feb. 15, 2017. [cited by applicant]