IP Library › Granted Patent US 12,734,218
Granted Patent B2
US 12,734,218 · App. 18/031,958 · Granted Sep 15, 2026

Use of trigonal agonist having activities to all of glucagon, GLP-1, and GIP receptors in treatment of sequelae following respiratory infectious diseases

Inventors: Jong Suk Lee (Hwaseong-si, KR); Jung Kuk Kim (Hwaseong-si, KR); Seon Myeong Lee (Hwaseong-si, KR); Sang Hyun Lee (Hwaseong-si, KR); Jeong A Kim (Hwaseong-si, KR); Euh Lim Oh (Hwaseong-si, KR); Chong Yoon Lim (Hwaseong-si, KR)
Assignee: HANMI PHARM. CO., LTD.
A61K38/26A61K47/6811A61P11/00
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Quick Facts
Patent No.
US 12,734,218
App. No.
18/031,958
Granted
Sep 15, 2026
Kind
B2
Abstract

Provided is use of a trigonal agonist having activities to all of glucagon, GLP-1, and GIP receptors, and/or a conjugate thereof in the prevention or treatment of sequelae following respiratory infectious diseases.

Claims (25)

1 . A method for treating sequelae following a respiratory infectious disease, comprising administering a pharmaceutical composition to a patient in need thereof, the pharmaceutical composition comprising a pharmaceutically acceptable excipient and a pharmaceutically effective amount of a peptide including any one amino acid sequence of SEQ ID NOS: 1 to 102.

2 . The method of claim 1 , wherein the peptide is in the form of a long-acting conjugate, and the long-acting conjugate is represented by the following Chemical Formula 1:

X-L-F  [Chemical Formula 1]

wherein X is a peptide of any one amino acid sequence of SEQ ID NOS: 1 to 102;

L is a linker including ethylene glycol repeating units,

F is an immunoglobulin Fc region, and

- represents a covalent linkage between X and L, and between L and F.

3 . The method of claim 1 , wherein the respiratory infectious disease is an infectious disease caused by respiratory virus.

4 . The method of claim 3 , wherein the respiratory virus is any one selected from the group consisting of adenovirus, vaccinia virus, herpes simplex virus, parainfluenza virus, rhinovirus, varicella zoster virus, measle virus, respiratory syncytial virus, Dengue virus, human immunodeficiency virus (HIV), influenza virus, coronavirus, severe acute respiratory syndrome associated virus (SARS-associated virus), and Middle East respiratory syndrome coronavirus (MERS-CoV).

5 . The method of claim 3 , wherein the respiratory virus is SARS-CoV-2.

6 . The method of claim 3 , wherein the respiratory virus is a variant respiratory virus.

7 . The method of claim 6 , wherein the variant respiratory virus causes sequelae the same as those caused by the respiratory virus.

8 . The method of claim 6 , wherein the variant respiratory virus is any one selected from the group consisting of SARS-CoV-2 alpha variant (B.1.1.7 lineage), SARS-CoV-2 beta variant (B.1.351 lineage), SARS-CoV-2 gamma variant (P.1 lineage), and SARS-CoV-2 delta variant (B.1.617.2 lineage).

9 . The method of claim 1 , wherein the sequelae following a respiratory infectious disease is any one or more selected from the group consisting of fever, dyspnea, cough, pneumonia, pulmonary fibrosis, pain, myalgia, fatigue, inflammation, and nervous system disorders.

10 . The method of claim 9 , wherein the sequelae following respiratory infectious disease is caused by tissue damage due to excessive cytokine secretion.

11 . The method of claim 1 , wherein the sequelae following respiratory infectious disease is post-COVID-19 pulmonary fibrosis.

12 . The method of claim 1 , wherein the administering of the pharmaceutical composition exhibits one or more of the followings:

(i) a reduction in the lung inflammation score;

(ii) a reduction in the expression or secretion of a pro-inflammatory cytokine cytokines;

(iii) a reduction in the pulmonary fibrotic area; and

(iv) suppressed production of inflammasome complexes.

13 . The method of claim 12 , wherein the pro-inflammatory cytokine is any one or more selected from the group consisting of interleukin, tumor necrosis factor, and interferon.

14 . The method of claim 12 , wherein the pro-inflammatory cytokine is IL-1β, TNF-α, or IFN-γ.

15 . The method of claim 1 , wherein the pharmaceutical composition is administered to an individual having cytokine storm syndrome, sepsis, or organ failure due to respiratory viral infection.

16 . The method of claim 1 , wherein the peptide includes an amino acid sequence selected from the group consisting of SEQ ID NOS: 21, 22, 42, 43, 50, 77, and 96.

Assignments (1)
ASSIGNMENT OF ASSIGNOR'S INTEREST Recorded Apr 14, 2023
From: LEE, JONG SUK; KIM, JUNG KUK; LEE, SEON MYEONG; LEE, SANG HYUN; KIM, JEONG A; OH, EUH LIM; LIM, CHONG YOON
To: HANMI PHARM. CO., LTD.
Reel/Frame 063325/0083 →
Priority Claims (2)
KR 10-2020-0134344 · Oct 16, 2020 · national
KR 10-2021-0028215 · Mar 3, 2021 · national
Continuity (1)
Related Publication 20230390362A1 · Dec 7, 2023
References Cited (22)
US 10370426B2 · Oh · 2019 [cited by examiner]
US 10400020B2 · Oh et al. · 2019 [cited by applicant]
US 20150322129A1 · Bossart et al. · 2015 [cited by applicant]
US 20170298117A1 · Hwang · 2017 [cited by examiner]
KR 1020170080522A · 2017 [cited by applicant]
KR 1020200038878A · 2020 [cited by applicant]
WO 2017116204A1 · 2017 [cited by applicant]
WO 2017116205A1 · 2017 [cited by applicant]
WO 2021145552A1 · 2021 [cited by applicant]
Ahmad et al. (Biochim Biophys Acta Mol Basis Dis. Jun. 13, 2020; 1866(10):165878). [cited by examiner]
Bloodworth et al. Letter to the Editor, vol. 142, Issue 2p. 683-687). [cited by examiner]
Deependra Kumar Rai, et al., Post covid 19 pulmonary fibrosis. Is it real threat?, Elsevier, Indian Journal of Tuberculosis, 2021, pp. 330-333, vol. 68. [cited by applicant]
Hye Soon Kim, “Management of Diabetes in Coronavirus Disease 2019: Prognosis and Practical Issues”, The Journal of Korean Diabetes, Sep. 2020, pp. 120-125, vol. 21, No. 3. [cited by applicant]
Ying Jie Chee, et al., “Dissecting the interaction between COVID-19 and diabetes mellitus”, JDI Journal of Diabetes Investigation, Official Journal of the Asian Association for the Study of Diabetes, Sep. 5, 2020, pp. 1… [cited by applicant]
International Search Report for PCT/KR2021/014485 dated Feb. 14, 2022. [cited by applicant]
Extended European Search Report issued Sep. 24, 2024 in Application No. 21880637.0. [cited by applicant]
Makarev, et al., “Common pathway signature in lung and liver fibrosis”, Cell Cycle, 2016, vol. 15, No. 13, pp. 1667-1673 (7 pages). [cited by applicant]
Liu, et al., “Application of nintedanib and other potential anti-fibrotic agents in fibrotic diseases”, Clin Sci (Lond), Jun. 28, 2019, vol. 133, No. 12, pp. 1309-1320 (20 pages). [cited by applicant]
Kim, et al., “Therapeutic effect of a novel long-acting GLP-1/GIP/Glucagon triple agonist (HM15211) in a NASH and fibrosis animal model”, American Diabetes Association (ADA) 79 [cited by applicant]
Kim, et al., “Therapeutic effect of a novel long-acting GLP-1/GIP/Glucagon triple agonist (HM15211) in NASH and fibrosis animal models”, Diabetologia, 2018, vol. 61, Suppl. 1, pp. S61-S62 (2 pages). [cited by applicant]
Bai et al., “The active GLP-1 analogue liraglutide alleviates H9N2 influenza virus-induced acute lung injury in mice”, Microbial Pathogenesis, 2021, vol. 150, No. 104645, pp. 1-12 (13 pages total). [cited by applicant]
Fandiño et al., “GLP-1 receptor agonist ameliorates experimental lung fibrosis”, Scientific Reports, 2020, vol. 10, No. 18091, pp. 1-15 (16 pages total). [cited by applicant]