Anti-il-5 antibody in the treatment of asthma

Abstract

Disclosed herein are antigen binding proteins, e.g. an antibody, which bind to IL-5, for use in the treatment of asthma, wherein the rate of exacerbations is reduced.

Description

[0001] ANTI-IL-5 ANTIBODY IN THE TREATMENT OF ASTHMA FIELD OF THE INVENTION The present invention relates to antigen binding proteins, e.g. an antibody, which bind to IL-5, for use in the treatment of asthma, wherein the rate of exacerbations is reduced. BACKGROUND TO THE INVENTION Asthma is a chronic heterogeneous lung disease characterised by inflammation, narrowing of the airways, and reversible airway obstruction. Patients with uncontrolled asthma suffer from continuing symptoms and acute exacerbations of the disease. Exacerbations are particularly disabling, necessitating patient treatment usually with oral / systemic corticosteroids. The frequency of asthma exacerbations appears to be closely related to eosinophil airway inflammation (FitzGerald & Gibson, Prevention. Thorax.2006; 61: 992-999). Persistent eosinophil inflammation is a feature of more than 50% of patients with severe asthma (Chung et al. Eur. Respir. J.2014; 43: 343-73). T2 inflammation, often identified by elevated blood eosinophil count, is the underlying pathology for more than 80% of people with severe asthma and can lead to unpredictable exacerbations (ERJOpen Res.2022;8:00576–2021; Eur Respir J.2022;60(2):2101865; Nat Rev Immunol.2013;13(1):9-22; Chest.2021;160(3):814-830). Several monoclonal antibodies targeting eosinophil inflammation have received marketing authorization for asthma with an eosinophilic phenotype, including 3 targeting either interleukin-5 (IL-5) or its receptor (IL- 5R): mepolizumab (Nucala), reslizumab (Cinqair) and benralizumab (Fasenra). All three, by utilizing blood eosinophils as a biomarker to predict patients likely to respond to therapy, have been shown to reduce asthma exacerbations, and improve lung function and health-related quality of life, in patients with asthma with an eosinophilic phenotype. IL-5 is a secreted protein. IL-5 plays a role in a number of different diseases such as asthma, mild asthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma, and sub-eosinophilic asthma. These diseases affect hundreds of millions of people worldwide. In light of the above, it is clear that there is a need for more effective treatments for asthma. SUMMARY OF THE INVENTION The invention provides an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 for use in the treatment of asthma in a patient, wherein the patient’s rate of exacerbations is reduced. The invention also provides an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQID NO: 10 for use in the treatment of asthma in a patient, wherein the patient’s SGRQscore is reduced. DETAILED DESCRIPTION OF THE INVENTION DEFINITIONS Unless defined otherwise, all technical and scientific terms used herein have the same meaning as commonly understood by one of ordinary skill in the art. The singular terms "a," "an," and "the" include plural referents unless context clearly indicates otherwise. Similarly, the word "or" is intended to include "and" unless the context clearly indicates otherwise. The term "plurality" refers to two or more. The term “at least one” refers to one or more. Additionally, numerical limitations given with respect to concentrations or levels ofa substance, such as solution component concentrations or ratios thereof, are intended tobe approximate. Unless specified otherwise, where a numerical range is provided, it is inclusive, i.e., the endpoints are included. "About" as used herein when referring to a measurable value such as an amount and the like, is meant to encompass variations of ±20% or ±10%, including ±5%, ±1%, and ±0.1% from the specified value, as such variations are appropriate to perform the disclosed methods. The term "antigen binding protein" as used herein refers to antibodies, antibody fragments and other protein constructs which are capable of binding to an antigen. The term “antibody” is used herein in the broadest sense to refer to molecules with an immunoglobulin-like domain (for example IgG, IgM, IgA, IgD or IgE) and includes monoclonal, recombinant, polyclonal, chimeric, human, humanised, multispecific antibodies, including bispecific antibodies, and heteroconjugate antibodies; a singlevariable domain (e.g. a domain antibody (DAB)), antigen binding antibody fragments, Fab,F(ab’)2, Fv, disulphide linked Fv, single chain Fv, disulphide-linked scFv, diabodies, TANDABS, etc. and modified versions of any of the foregoing (for a summary of alternative “antibody” formats see Holliger and Hudson, Nature Biotechnology, 2005, Vol 23, No.9, 1126-1136). Alternative antibody formats are also contemplated and include alternative scaffolds in which the one or more CDRs of the antigen binding protein can be arranged onto a suitable non-immunoglobulin protein scaffold or skeleton, such as an affibody, a SpA scaffold, an LDL receptor class A domain, an avimer or an EGF domain.The antibody may be derived from rat, mouse, primate (e.g., cynomolgus, Old Worldmonkey or Great Ape), human or other sources such as nucleic acids generated using molecular biology techniques which encode an antibody molecule. The antigen binding protein may comprise a constant region, which may be of anyisotype or subclass. The constant region may be of the IgG isotype, for example, IgG1, IgG2, IgG3, IgG4 or variants thereof. The antigen binding protein constant region may be IgG1. The antigen binding protein may comprise one or more modifications selected from a mutated constant domain such that the antibody has enhanced effector functions / ADCC and / or complement activation. The antigen binding proteins of the invention can be used in any of the pharmaceutical compositions, dosage regimens, or method of treatments of the invention. The antigen binding proteins can be antibodies, for example IgG1antibodies. The term “interleukin-5” or “IL-5” as used herein includes human IL-5 comprising the amino acid sequence shown in SEQ ID NO: 11. The term “interleukin-5 receptor” or “IL-5R” as used herein includes human IL-5 Receptor Subunit Alpha Isoform 1 comprising the amino acid sequence shown in SEQ ID NO: 12. The term “binds”, as used herein in relation to antigen binding proteins means that the antigen binding protein binds to a target antigen as well as a discrete domain, or discrete amino acid sequence, within a target antigen with no or insignificant binding to other (for example, unrelated) proteins. This term, however, does not exclude the fact that the antigen binding proteins may also be cross-reactive with closely related molecules (for example, those with a high degree of sequence identity or from another genera or species). The antigen binding proteins described herein may bind to human IL-5 with at least 2, 5, 10, 50, 100, or 1000-fold greater affinity than they bind to closely related molecules. By “isolated”, it is intended that the molecule, such as an antigen binding protein, is removed from the environment in which it may be found in nature. For example, the molecule may be purified away from substances with which it would normally exist in nature. The terms “VH” and “VL” are used herein to refer to the heavy chain variable region and light chain variable region, respectively, of an antigen binding protein. “CDRs” are defined as the complementarity determining region amino acid sequences of an antigen binding protein. These are the hypervariable regions of immunoglobulin heavy and light chains. There are three heavy chain and three light chain CDRs (or CDR regions) in the variable portion of an immunoglobulin. Thus, "CDRs" as used herein refers to all three heavy chain CDRs, all three light chain CDRs, all heavy and light chain CDRs, or at least one CDR and wherein the at least one CDR is CDRH3. Framework regions follow each of these CDR regions. Acceptable heavy chain variable region and light chain variable region framework 1, framework 2 and framework 3 regions are readily recognized by those of ordinary skill in the art. Acceptable heavy chain constant regions (including hinge regions) and light chain constant regions are readily recognized by those of ordinary skill in the art as well. Acceptable antibody isotypes are similarly readily recognized by those of ordinary skill in the art. Throughout this specification, amino acid residues in variable domain sequences and full length antibody sequences are numbered according to the Kabat numbering convention. Similarly, the terms “CDR”, “CDRL1”, “CDRL2”, “CDRL3”, “CDRH1”, “CDRH2”, “CDRH3” used in the specification follow the Kabat numbering convention. It will be apparent to those skilled in the art that there are alternative numbering conventions for amino acid residues in variable domain sequences and full length antibody sequences. There are also alternative numbering conventions for CDR sequences, for example those set out according to the Chothia numbering convention. The structure and protein folding of the antibody may mean that other residues are considered part of the CDR sequence and would be understood to be so by a skilled person. Other numbering conventions for CDR sequences available to a skilled person include “AbM” (University of Bath) and “contact” (University College London) methods. The minimum overlapping region using at least two of the Kabat, Chothia, AbM and contact methods can be determined to provide the “minimum binding unit”. The minimum binding unit may be a sub-portion of a CDR. The term “asthma” as used herein means an inflammatory disease of the airways characterized by reversible airflow obstruction and bronchospasm. Common symptoms include wheezing, coughing, chest tightness, and shortness of breath. Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation. Adiagnosis of asthma in a subject may be made according to the guidanceprovided by the Global Initiative for Asthma (GINA) the Global Strategy for Asthma Management and Prevention (2016 update) document. Those of ordinary skill in the art will be familiar with the GINA diagnostic flow chart for clinical practice and diagnostic criteria for asthma in adults, adolescents and children 6-11 years (Table 1) shown belowas well as other aspect of the guidance (e.g., for pregnant women etc.). See also Table 2and Table 3. Table 1. Box 1-2. Diagnostic criteria for asthma in adults, adolescents, and children 6–11 years. Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation. DIAGNOSTIC FEATURE DIAGNOSTIC FEATURE1. History of variable respiratory symptoms Wheeze, shortness of breath, chest tightness • Generally more than one type of respiratory and cough symptom (in adults, isolated cough is seldom Descriptors may vary between cultures and by due to asthma) age, e.g. children may be described as having • Symptoms occur variably over time and vary heavy breathing in intensity • Symptoms are often worse at night or on waking • Symptoms are often triggered by exercise, laughter, allergens, cold air • Symptoms often appear or worsen with viral infections 2. Confirmed variable expiratory airflow limitation Documented excessive variability in lung The greater the variations, or the more function* (one or more of the tests below) occasions excess variation is seen, the more AND documented airflow limitation* confident the diagnosis At least once during diagnostic process when FEV1 is low, confirm that FEV1 / FVC is reduced (normally >0.75–0.80 in adults, >0.90 in children) Positive bronchodilator (BD) reversibility test* Adults: increase in FEV1 of >12% and >200 (more likely to be positive if BD medication is mL from baseline, 10–15 minutes after 200– withheld before test: SABA ≥4 hours, LABA 400 mcg albuterol or equivalent (greater ≥15 hours) confidence if increase is >15% and >400 mL). Children: increase in FEV1 of >12% predicted Excessive variability in twice-daily PEF over 2 Adults: average daily diurnal PEF variability weeks* >10%** Children: average daily diurnal PEF variability >13%** Significant increase in lung function after 4 Adults: increase in FEV1 by >12% and >200 weeks of anti-inflammatory treatment mL (or PEF† by >20%) from baseline after 4 weeks of treatment, outside respiratory infectionsPositive exercise challenge test* Adults: fall in FEV1 of >10% and >200 mLfrom baseline Children: fall in FEV1 of >12% predicted, or PEF >15% Positive bronchial challenge test (usually only Fall in FEV1 from baseline of ≥20% with performed in adults) standard doses of methacholine or histamine, or ≥15% with standardized hyperventilation, hypertonic saline or mannitol challenge Excessive variation in lung function between Adults: variation in FEV1 of >12% and >200 visits* (less reliable) mL between visits, outside of respiratory infections Children: variation in FEV1 of >12% in FEV1 or >15% in PEF† between visits (may include respiratory infections) BD: bronchodilator (short-acting SABA or rapid-acting LABA); FEV1: forced expiratory volume in 1 second; LABA: long-acting beta2-agonist; PEF: peak expiratory flow (highest of three readings); SABA: short-acting beta2-agonist. See Box 1-4 for diagnosis in patients already taking controller treatment. *These tests can be repeated during symptoms or in the early morning. **Daily diurnal PEF variability is calculated from twice daily PEF as ([day’s highest minus day’s lowest] / mean of day’s highest and lowest), and averaged over one week. †For PEF, use the same meter each time, as PEF may vary by up to 20% between different meters. BD reversibility may be lost during severe exacerbations or viral infections. If bronchodilator reversibility is not present at initial presentation, the next step depends on the availability of other tests and the urgency of the need for treatment. In a situation of clinical urgency, asthma treatment may be commenced and diagnostic testing arranged within the next few weeks (Box 1-4), but otherconditions that can mimic asthma (Box 1-3) should be considered, and the diagnosis of asthmaconfirmed as soon as possible.

[0002] Table 2. Box 1-3. Differential diagnosis of asthma in adults, adolescents and children 6–11 years.Age Condition Symptoms6–11 years Chronic upper airway coughSneezing, itching, blocked nose, throat- syndrome clearing Inhaled foreign body Sudden onset of symptoms, unilateral wheeze Bronchiectasis Recurrent infections, productive cough Recurrent infections, productive cough, Primary ciliary dyskinesia sinusitis Cardiac murmurs Congenital heart disease Pre-term delivery, symptoms since Bronchopulmonary dysplasia birth Excessive cough and mucus Cystic fibrosis production, gastrointestinal symptoms 12–39 Chronic upper airway cough Sneezing, itching, blocked nose, throat- syndrome clearing years Vocal cord dysfunction Dyspnea, inspiratory wheezing (stridor) Dizziness, paresthesia, sighing Hyperventilation, dysfunctional breathing Productive cough, recurrent infections Bronchiectasis Excessive cough and mucus production Cystic fibrosis Cardiac murmurs Shortness of breath, family history of early emphysema Congenital heart disease Sudden onset of symptoms Alpha1-antitrypsin deficiency Inhaled foreign body40+ years Vocal cord dysfunctionDyspnea, inspiratory wheezing (stridor) Dizziness, paresthesia, sighing Hyperventilation, dysfunctional breathing Cough, sputum, dyspnea on exertion, COPD* smoking or noxious exposure Productive cough, recurrent infections Bronchiectasis Dyspnea with exertion, nocturnal symptoms Cardiac failure Treatment with angiotensin converting enzyme (ACE) inhibitor Medication-related cough Dyspnea with exertion, non-productive cough, finger clubbing Parenchymal lung disease Sudden onset of dyspnea, chest pain Dyspnea, unresponsive to bronchodilators Pulmonary embolism Central airway obstruction *Any of the above conditions may also contribute to respiratory symptoms in patients with confirmed asthma. Table 3. Box 1-4. Confirming the diagnosis of asthma in a patient already taking controller treatment.Current status Steps to confirm the diagnosis of asthmaVariable respiratory symptoms and Diagnosis of asthma is confirmed. Assess the level variable airflow limitation of asthma control and review controller treatment. Variable respiratory symptoms but no Repeat BD reversibility test again after variable airflow limitation withholding BD (SABA: 4 hours; LABA: 12+ hours) or during symptoms. If normal, consider alternative diagnoses (Box 1-3). If FEV1 is >70% predicted: consider a bronchial provocation test. If negative, consider stepping down controller treatment and reassess in 2–4 weeks If FEV1 is <70% predicted: consider stepping up controller treatment for 3 months, then reassess symptoms and lung function. If no response, resume previous treatment and refer patient for diagnosis and investigation Few respiratory symptoms, normal lung Repeat BD reversibility test again after function, and no variable airflow limitation withholding BD (SABA: 4 hours; LABA: 12+ hours) or during symptoms. If normal, consider alternative diagnoses (Box 1-3). Consider stepping down controller treatment: • If symptoms emerge and lung function falls: asthma is confirmed. Step up controller treatment to lowest previous effective dose. • If no change in symptoms or lung function at lowest controller step: consider ceasing controller, and monitor patient closely for at least 12 months. Persistent shortness of breath and fixed Consider stepping up controller treatment for 3 airflow limitation months, then reassess symptoms and lung function. If no response, resume previous treatment and refer patient for diagnosis and investigation. Consider asthma–COPD overlap syndrome. BD: bronchodilator; LABA: long-acting beta2-agonist; SABA: short-acting beta2-agonist As used herein, in an embodiment, “asthma” may be “mild asthma,” “moderate asthma” or “severe asthma.” Asthma severity can be assessed according to the GINA guidance. In particular, asthma severity can be assessed retrospectively from the level of treatment required to control symptoms and exacerbations. For example, it can be assessed once the patient has been on controller treatment for several months and, if appropriate, treatment step down has been attempted to find the patient’s minimum effective level of treatment. Asthma severity is not a static feature and may change over months or years. Asthma severity can be assessed when the patient has been on regular controller treatment for several months: •“Mild asthma” is asthma that is well controlled with Step 1 or Step 2 treatment(see Figure 9 of WO2018215964), i.e., with as-needed reliever medication alone, or with low-intensity controller treatment such as low dose ICS, leukotriene receptor antagonists or chromones. •“Moderate asthma” is asthma that is well controlled with Step 3 treatment (seeFigure 9 of WO2018215964), e.g., low dose ICS / LABA. •“Severe asthma” is asthma that requires Step 4 or 5 treatment (see Figure 9 ofWO2018215964), e.g., high-dose ICS / LABA, to prevent it from becoming ‘uncontrolled’, or asthma that remains ‘uncontrolled’ despite this treatment. While many patients with uncontrolled asthma may be difficult to treat due to inadequate or inappropriate treatment, or persistent problems with adherence or comorbidities such as chronic rhinosinusitis or obesity, the European Respiratory Society / American Thoracic Society Task Force on Severe Asthmaconsidered that the definition of “severe asthma” should be reserved for patients with refractory asthma and those in whom response to treatment of comorbidities is incomplete. Table 4 can also be referred to during the assessment of asthma severity. Table 4. Box 3-6. Low, medium and high daily doses of inhaled corticosteroids. Drug Daily dose (mcg)Low Medium HighBeclometasone dipropionate (CFC)* 200–500 >500–1000 >1000 Beclometasone dipropionate (HFA) 100–200 >200–400 >400 Budesonide (DPI) 200–400 >400–800 >800 Ciclesonide (HFA) 80–160 >160–320 >320 Fluticasone furoate (DPI) 100 n.a. 200 Fluticasone propionate(DPI) 100–250 >250–500 >500 Fluticasone propionate (HFA) 100–250 >250–500 >500 Mometasone furoate 110–220 >220–440 >440 Triamcinolone acetonide 400–1000 >1000–2000 >2000 Children 6–11 years (for children 5 years and younger) Beclometasone dipropionate (CFC)* 100–200 >200–400 >400 Beclometasone dipropionate (HFA) 50-100 >100-200 >200 Budesonide (DPI) 100–200 >200–400 >400 Budesonide (nebules) 250–500 >500–1000 >1000 Ciclesonide 80 >80-160 >160 Fluticasone furoate (DPI) n.a. n.a. n.a. Fluticasone propionate (DPI) 100–200 >200–400 >400 Fluticasone propionate (HFA) 100–200 >200–500 >500 Mometasone furoate 110 ≥220–<440 ≥440 Triamcinolone acetonide 400–800 >800–1200 >1200 CFC: chlorofluorocarbon propellant; DPI: dry powder inhaler; HFA: hydrofluoroalkane propellant; n.a. not applicable *Beclometasone dipropionate CFC is included for comparison with older literature As used herein, in another embodiment, “asthma” may be “mild eosinophilic asthma,” “moderate eosinophilic asthma,” or “severe eosinophilic asthma.” “Mild eosinophilic asthma” is mild asthma with an eosinophilic phenotype. For example, subjects with mild eosinophilic asthma may have mild asthma and blood eosinophils (e.g., blood eosinophil count (BEC)) greater than or equal to 150 eosinophils per μL of blood in the past 12 months, greater than or equal to 200 eosinophils per μL of blood in the past 12 months, greater than or equal to 300 eosinophils per μL of blood in the past 12 months or greater than or equal to 350 eosinophils per μL of blood in the past 12 months. “Moderate eosinophilic asthma” is moderate asthma with an eosinophilic phenotype. For example, subjects with moderate eosinophilic asthma may have moderate asthma and blood eosinophils (e.g., blood eosinophil count (BEC)) greater than or equal to 150 eosinophils per μL of blood in the past 12 months, greater than or equal to 200 eosinophils per μL of blood in the past 12 months, greater than or equal to 300 eosinophils per μL of blood in the past 12 months or greater than or equal to 350 eosinophils per μL of blood in the past 12 months. “Severe eosinophilic asthma” is severe asthma with an eosinophilic phenotype. For example, subjects with severe eosinophilic asthma may have severe asthma and blood eosinophils (e.g., blood eosinophil count (BEC)) greater than or equal to 150 eosinophils per μL of blood in the past 12 months, greater than or equal to 200 eosinophils per μL of blood in the past 12 months, greater than or equal to 300 eosinophils per μL of blood in the past 12 months (preferred) or greater than or equal to 350 eosinophils per μL of blood in the past 12 months. Subjects with severe eosinophilic asthma may also meet, one or more of the criteria described in Table 5. Table 5. A subject has severe eosinophilic asthma if they meet the following criteria: 1) The subject has clinical features of severe refractory asthma similar to those indicated in the American Thoracic Society Workshop on Refractory Asthma (162, Am. J. Respir. Crit. Care Med. 2341 (2000)) for ≥12 months. 2) The subject has a well-documented requirement for regular treatment with high dose ICS (inhaled corticosteroids) (i.e., ≥880 μg / day fluticasone propionate or equivalent daily), with or without maintenance OCS (oral corticosteroids), in the past 12 months. 3) The subject has a well-documented requirement for controller medication, e.g., long-acting beta-2-agonist, leukotriene receptor antagonist or theophylline in the past 12 months. 4) The subject has persistent airflow obstruction as indicated by a pre-bronchodilator FEV1 <80% predicted recorded or peak flow diurnal variability of >20% on 3 or more days. 5) The subject has airway inflammation which is likely to be eosinophilic in nature as indicated by one of the following characteristics at present or documented in the previous 12 months: ‒An elevated peripheral blood eosinophil level of ≥300 / μL that is related to asthma or‒ Sputum eosinophils ≥3% or‒ Exhaled nitric oxide ≥50 ppb or‒ Prompt deterioration of asthma control (based on documented clinical history or objectivemeasures) following a ≤25% reduction in regular maintenance dose of inhaled or oral corticosteroid dose in the previous 12 months 8) The subject has a previously confirmed history of two or more asthma exacerbations requiring treatment with oral or systemic corticosteroids in the prior 12 months prior, despite the use of high-dose ICS and additional controller medication. For subjects receiving maintenance OCS with high-dose ICS plus controller, the OCS treatment for exacerbations had to be a two-fold or greater increase in the dose of OCS. 9) The subject has asthma as documented by either: ‒Airway reversibility (FEV1 ≥12% and 200 mL) at present or documented in the previous 12months or ‒Airway hyper-responsiveness (provocative concentration causing a 20% fall in FEV1 ofmethacholine <8 mg / mL or provocative dose causing a 20% fall in FEV1 of histamine <7.8 μmol) documented in the prior 12 months or ‒Airflow variability in clinic FEV1 ≥20% between two examinations documented in the prior 12months (FEV1 recorded during an exacerbation is not valid) or ‒Airflow variability as indicated by >20% diurnal variability in peak flow observed on 3 ormore days. Importantly, subjects with severe eosinophilic asthma according to these criteria in Table 5 may have less than 150 eosinophils per μL of blood at the initiation of treatment. The term “pharmaceutical composition” as used herein means a composition suitable for administration to a patient. The term “therapeutically effective amount” as used herein means an amount of an agent (such as an antigen binding protein or a pharmaceutical composition), which provides a therapeutic benefit in the treatment or management of one or more symptoms of a condition to be treated (such as asthma, mild asthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma and sub-eosinophilic asthma). Examples of such treatment or management of one or more symptoms of asthma—including asthma, mild asthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma and sub-eosinophilic asthma— include 1) a reduction of the frequency of asthma exacerbations; 2) a reduction in the time to first clinically significant exacerbation requiring oral or systemic corticosteroids, hospitalisation, and / or emergency department (ED) visits; 3) a reduction in the frequency of exacerbations requiring hospitalization (including intubation and admittance to an intensive care unit) or ED visits; 4) a reduction in the time to first exacerbation requiring hospitalization or ED visit; 5) a change from baseline in clinic pre-bronchodilator FEV1; 6) a change from baseline in clinic post-bronchodilator FEV1; 7) a change from baseline in an Asthma Control Questionnaire (ACQ) score; 8) improved lung function as assessed by spirometry (e.g., vital capacity (VC), forced vital capacity (FVC), forced expiratory volume (FEV) at timed intervals of 0.5, 1.0 (FEV1), 2.0, and 3.0 seconds, forced expiratory flow 25–75% (FEF 25–75) and maximal voluntary ventilation (MVV) total lung capacity, idal volume, residual volume, expiratory reserve volume, inspiratory reserve volume, inspiratory capacity, inspiratory vital capacity, vital capacity, functional residual capacity, residual volume expressed as percent of total lung capacity, alveolar gas volume, actual volume of the lung including the volume of the conducting airway, forced vital capacity, etc.); and 9) a reduction in asthma exacerbations requiring steroids for control (such as oral steroids or steroids, such as prednisone, prednisolone etc., administered by any route). Such a reduction in asthma exacerbations requiring steroids for control may be an approximately 50% reduction in exacerbations requiring steroids (e.g., oral steroids). Therapeutically effective amounts and treatment regimens are generally determined empirically and may be dependent on factors, such as the age, weight, and health status of the patient and disease or disorder to be treated. Such factors are within the purview of the attending physician. As used herein, the term “treatment” refers to ameliorating or stabilising the specified condition, reducing or eliminating the symptoms of the condition, slowing or eliminating the progression of the condition, and preventing or delaying reoccurrence of the condition in a previously afflicted patient or subject. As is recognised in the art, drugs employed as therapeutic agents in methods of treatment may reduce the severity of a given disease state, but need not abolish every manifestation of the disease to be regarded as useful therapeutic agents. Simply reducing the impact of a disease (for example, by reducing the number or severity of its symptoms, or by increasing the effectiveness of another treatment, or by producing another beneficial effect), or reducing the likelihood that the disease will occur (for example by delaying the onset of the disease) or worsen in a subject, is sufficient. As used herein, the term "patient" refers to a human. The terms “individual”,“subject” and “patient” are used herein interchangeably. The patient may be an adult oradolescent (≥12 years). As used herein, the phrase “once every 6 months” means that in a typical 6 month period consisting of about 183 days, a subject is administered a dose of the antigen binding protein of the invention on one day only and on the other days the subject is not administered a dose of the antigen binding protein of the invention. Administration of once every 6 months may also be referred to as “Q26W” (which refers to administration once every 26 weeks). References herein to “about once every 6 months” refer to an intended dosage regime of once every 6 months, but with the allowance of patient compliance, therefore allowing up to a four week variation depending upon patient scheduling. As used herein, the term “annualised rate of exacerbations” or “annualised rate of clinically significant exacerbations” refers to the number of asthma exacerbations or the number of clinically significant asthma exacerbations that occur over a year (i.e., 52-week period). In some cases where the patient follow-up period is more or less than 52 weeks, the number of asthma exacerbations is normalized to an annual rate. If desired, the effective dose of an antibody or antigen binding protein of the disclosure (e.g., as a pharmaceutical composition) may be administered as a unit dosage form. STATEMENT OF THE INVENTION The present invention includes an antigen binding protein which binds to humanIL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequenceshown in SEQ ID NO: 10 for use in the treatment of asthma in a patient, wherein thepatient’s rate of exacerbations is reduced. In one embodiment, the patient’s annualisedrate of exacerbations is reduced. In one embodiment, the patient’s annualised rate ofclinically significant exacerbations is reduced. In one embodiment, the patient’sannualised rate of clinically significant exacerbations over 52 weeks is reduced. In oneembodiment, the patient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced compared to placebo.The present invention includes a method of treating asthma comprisingadministering to a patient an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10, wherein the patient’s rate of exacerbations is reduced. In one embodiment, the patient’s annualised rate of exacerbations is reduced. In one embodiment, the patient’sannualised rate of clinically significant exacerbations is reduced. In one embodiment, thepatient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced. In one embodiment, the patient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced compared to placebo. The present invention includes an antigen binding protein which binds to humanIL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequenceshown in SEQ ID NO: 10 for use in a method of reducing the rate of exacerbations in a patient with asthma. In one embodiment, the annualised rate of exacerbations is reduced.In one embodiment, the annualised rate of clinically significant exacerbations is reduced.In one embodiment, the annualised rate of clinically significant exacerbations over 52weeks is reduced. In one embodiment, the annualised rate of clinically significantexacerbations over 52 weeks is reduced compared to placebo. The present invention also includes a method of reducing the rate of exacerbationsin a patient with asthma comprising administering to the patient an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown inSEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acidsequence shown in SEQ ID NO: 10. In one embodiment, the annualised rate ofexacerbations is reduced. In one embodiment, the annualised rate of clinically significant exacerbations is reduced. In one embodiment, the annualised rate of clinically significant exacerbations over 52 weeks is reduced. In one embodiment, the annualised rate of clinically significant exacerbations over 52 weeks is reduced compared to placebo. The annualised rate of exacerbations may be reduced by at least 10%, at least20%, at least 30%, at least 40%, at least 50%, at least 60%, at least 65%, at least 70% orat least 80%. The annualised rate of exacerbations may be reduced by at least 45%, atleast 50%, at least 55%, at least 60%, at least 65%, at least 70% or at least 80%. In oneembodiment, the annualised rate of exacerbations is reduced by at least 45%. In one embodiment, the annualised rate of exacerbations is reduced by at least 48%. In one embodiment, the annualised rate of exacerbations is reduced by at least 50%. In one embodiment, the annualised rate of exacerbations is reduced by at least 54%. In one embodiment, the annualised rate of exacerbations is reduced by at least 55%. The annualised rate of exacerbations may be reduced by at least 58%. The annualised rate of exacerbations may be reduced by at least 60%. The annualised rate of exacerbations may be reduced by at least 64%. The annualised rate of exacerbations may be reduced by at least 66%. The annualised rate of exacerbations may be reduced by at least 68%. The annualised rate of exacerbations may be reduced by at least 70%. The annualised rate ofexacerbations may be reduced by at least 71%. The annualised rate of exacerbations maybe reduced by at least 74%. The annualised rate of exacerbations may be reduced by atleast 80%. The annualised rate of exacerbations may be reduced by at least 84%. Theannualized rate of exacerbations may refer to the patient’s annualized rate ofexacerbations. The annualised rate of exacerbations may be reduced as compared to thenumber of exacerbations expected according to the patient’s history, as compared to the average number of exacerbations expected in a comparable population of patients, or as compared to a comparable population treated with placebo over the same time period. The annualised rate of exacerbations may be reduced as compared to a comparablepopulation treated with placebo over the same time period.The annualised rate of exacerbations may be the annualised rate of clinicallysignificant exacerbations. Clinically significant exacerbations of asthma is defined asworsening of asthma which requires use of systemic corticosteroids and / or hospitalization and / or Emergency Department (ED) visit. The annualised rate of clinically significant exacerbations may be reduced by at least 10%, at least 20%, at least 30%, at least 40%,at least 50%, at least 60%, at least 65%, or at least 70% or at least 80%. The annualisedrate of clinically significant exacerbations may be reduced by at least 45%, at least 50%,at least 55%, at least 60%, at least 65%, at least 70% or at least 80%. In oneembodiment, the annualised rate of clinically significant exacerbations is reduced by atleast 45%. In one embodiment, the annualised rate of clinically significant exacerbations isreduced by at least 48%. In one embodiment, the annualised rate of clinically significantexacerbations is reduced by at least 50%. In one embodiment, the annualised rate of clinically significant exacerbations is reduced by at least 54%. In one embodiment, the annualised rate of clinically significant exacerbations is reduced by at least 55%. The annualised rate of exacerbations may be reduced by at least 58%. The annualised rate of clinically significant exacerbations may be reduced by at least 60%. The annualised rate of clinically significant exacerbations may be reduced by at least 64%. The annualised rate of exacerbations may be reduced by at least 66%. The annualised rate of clinically significant exacerbations may be reduced by at least 68%. The annualised rate of clinically significant exacerbations may be reduced by at least 70%. The annualised rate of clinically significant exacerbations may be reduced by at least 71%. The annualisedrate of clinically significant exacerbations may be reduced by at least 74%. Theannualised rate of clinically significant exacerbations may be reduced by at least 80%. The annualised rate of clinically significant exacerbations may be reduced by at least84%. The annualized rate of clinically significant exacerbations may refer to the patient’sannualized rate of clinically significant exacerbations. The annualised rate of clinically significant exacerbations may be reduced as compared to the number of exacerbations expected according to the patient’s history, as compared to the average number of exacerbations expected in a comparable population of patients, or as compared to acomparable population treated with placebo over the same time period. The annualisedrate of clinically significant exacerbations may be reduced as compared to a comparable population treated with placebo over the same time period. In one embodiment, the antigen binding protein which binds to human IL-5comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 is for use in the treatment of asthma in a patient, wherein the patient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced by at least 55% compared to placebo, optionally reduced by about 58%, and wherein the antigen binding protein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months. In one embodiment, the antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 is for use in the treatment of asthma in a patient, wherein the patient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced by at least 45% compared to placebo, optionally reduced by about 48%, and wherein the antigen binding protein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months. In one embodiment, the antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 is for use in the treatment of asthma in a patient, wherein the patient’s annualised rate of clinically significant exacerbations over 52 weeks is reduced by at least 50% compared to placebo, optionally reduced by about 54%, and wherein the antigen binding protein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months. In one embodiment, the antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 is for use in the treatment of asthma in a patient, wherein the patient’s annualised rate of exacerbations requiring hospitalisations and / or emergency department (ED) visits is reduced. In one embodiment, the patient’s annualised rate of exacerbations requiring hospitalisations and / or Emergency Department (ED) visits over 52 weeks is reduced. In one embodiment, the patient’s annualised rate of exacerbations requiringhospitalisations and / or Emergency Department (ED) visits is reduced by 70%, optionally72%. In one embodiment, the patient’s annualised rate of exacerbations requiring hospitalisations and / or Emergency Department (ED) visits is reduced by 70% compared to placebo, optionally reduced by 72%, and wherein the antigen binding protein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.2-1.0. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.2-0.7. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.3-0.6. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.44-0.70. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.37-0.58. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.5. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.56. In one embodiment, the annualised rate of clinically significant exacerbations is reduced to about 0.46.In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.5-3.5. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.5-3.0. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.5-2.0. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.7-2.0. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 1.0-2.0. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.7-1.6. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.8-1.5. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 0.83-1.41. In one embodiment, the annualised rate of clinically significantexacerbations prior to treatment is about 0.86-1.43. In one embodiment, the annualisedrate of clinically significant exacerbations prior to treatment is about 1.10. In oneembodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 1.08. In one embodiment, the annualised rate of clinically significant exacerbations prior to treatment is about 1.11. The disclosure provides an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQID NO: 10 for use in the treatment of asthma in a patient, wherein the patient’s SGRQscore is reduced. The SGRQ is a 51-item patient-reported outcome instrument to measure Quality of Life in participants with diseases of airway obstruction. It consists of two parts: Part 1 evaluating the symptom score and Part 2 measuring the activity and impact score. A Total score is calculated by summarizing the impact of the disease on overall health status. Scores are expressed as a percentage of overall impairment where 100 representing worst possible health status and 0 indicating best possible health status. Higher scores indicating greater impairment of quality of life. In one embodiment, the patient’s SGRQscore is reduced by at least 4 units, at least 5 units, at least 6 units, at least 7 units, at least 8 units or at least 9 units. In one embodiment, the patient’s SGRQ score is reduced by at least 4 units. In one embodiment, the patient’s SGRQ score is reduced by at least 5 units. In one embodiment, the patient’s SGRQ score is reduced by at least 6 units. In oneembodiment, the patient’s SGRQ score is reduced by at least 7 units. In one embodiment,the patient’s SGRQ score is reduced by at least 8 units. In one embodiment, the patient’s SGRQ score is reduced by at least 9 units. In one embodiment, the SGRQ score reduction is based on change from baseline in SGRQ total score at week 52. Change from Baseline is defined as value at the indicated time point minus Baseline value. The SGRQscore reduction may be reduced as compared to the score expected according to thepatient’s history, as compared to the score expected in a comparable population of patients, or as compared to a comparable population treated with placebo over the sametime period. The SGRQ score reduction may be reduced as compared to a comparablepopulation treated with placebo over the same time period. In one embodiment, the antigen binding protein comprises a heavy chain variable region sequence having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity to the amino acid sequence shown in SEQ ID NO: 3; and / or a light chain variable region sequence having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity the amino acid sequence shown in SEQ ID NO: 4. In one embodiment, the antigen binding protein comprises a heavy chain variable region sequence having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity to the amino acid sequence shown in SEQ ID NO: 3; and / or a light chain variable region sequence having at leastabout 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%,98.5%, 99%, 99.5%, 100% identity the amino acid sequence shown in SEQ ID NO: 4,wherein the heavy chain variable region has the CDRH1 amino acid sequence shown inSEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and theCDRH3 amino acid sequence shown in SEQ ID NO: 7; and the light chain variable regionhas the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acidsequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQID NO: 10. In one embodiment, the antigen binding protein comprises a heavy chainvariable region sequence having the amino acid sequence shown in SEQ ID NO: 3; and a light chain variable region sequence having the amino acid sequence shown in SEQ ID NO: 4. The antigen binding protein may comprise an Fc domain. The antigen binding protein may comprise a heavy chain Fc domain. The antigen binding protein maycomprise an IgG1, IgG2, IgG3 or IgG4 Fc domain. The antigen binding protein maycomprise a human IgG1, IgG2, IgG3 or IgG4 Fc domain. The antigen binding protein maycomprise an IgG1 Fc domain. The antigen binding protein may comprise a human IgG1 Fc domain. The antigen binding protein may also comprise a heavy chain Fc domain (e.g.,an IgG1 Fc) comprising a tyrosine residue at position 252, a threonine residue at position254 and a glutamic acid residue at position 256. The antigen binding protein may comprise a human IgG1 Fc domain comprising a tyrosine residue at position 252, a threonine residue at position 254 and a glutamic acid residue at position 256. The numbering of the amino acids in the heavy chain Fc domain (i.e., a tyrosine residue at position 252, a threonine residue at position 254 and a glutamic acid residue at position256) was derived using EU numbering, as described in: Edelman et al. (1969) Proc. Natl.Acad. USA, 63: 78-85 [PMID: 5257969]. The antigen binding protein may comprise ahuman IgG1 Fc domain comprising a tyrosine residue at position 252 (EU numbering), a threonine residue at position 254 (EU numbering) and a glutamic acid residue at position 256 (EU numbering). The antigen binding protein may further comprise a heavy chain FR4 amino acid sequence as shown in SEQ ID NO: 13. In one embodiment, the antigen binding protein comprises a heavy chain having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity to the amino acid sequence shown in SEQ ID NO: 1 and a light chain having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity the amino acid sequence shown in SEQ ID NO: 2. In one embodiment, the antigen binding protein comprises a heavy chain having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity to the amino acid sequence shown in SEQ ID NO: 1 and a light chain having at least about 90% identity for example about 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 98.5%, 99%, 99.5%, 100% identity the amino acid sequence shown in SEQ ID NO: 2, wherein the heavy chain has the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7;and the light chain has the CDRL1 amino acid sequence shown in SEQ ID NO: 8, theCDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10. In one embodiment, the antigen binding protein of the invention is an antibody comprising a heavy chain having the amino acid sequence shown in SEQ ID NO: 1 and a light chain having the amino acid sequence shown in SEQ ID NO: 2. In one embodiment, the antigen binding protein is depemokimab. In one embodiment, the antigen binding protein may be formulated within a pharmaceutical composition. In one embodiment, the pharmaceutical composition comprises the antigen binding protein and a pharmaceutically acceptable excipient. In one embodiment, the pharmaceutical composition comprises the antigen binding protein andan aqueous liquid formulation at about pH 6.0 comprising about 20 mM histidine, about180 mM trehalose, about 40 mM arginine, about 0.05 mM EDTA and about 0.02% weight of polysorbate 80 to volume. In one embodiment, the antigen binding protein is for use in the treatment ofasthma in a patient. The asthma may be selected from the group consisting of mildasthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma and sub-eosinophilic asthma. In a further embodiment, the asthma has an eosinophilic phenotype, e.g., mild eosinophilic asthma, moderate eosinophilic asthma or severe eosinophilic asthma. In one embodiment, the asthma is moderate asthma or severe asthma. In one embodiment, the asthma is moderate eosinophilic asthma or severe eosinophilic asthma. In one embodiment, the asthma is moderate asthma. In one embodiment, the asthma is moderate eosinophilic asthma. In one embodiment, the asthma is severe asthma. In one embodiment, the asthma is severeeosinophilic asthma. In one embodiment, the asthma is severe asthma with aneosinophilic phenotype. In one embodiment, the asthma is severe asthma with an eosinophilic phenotype characterized by blood eosinophil count ≥300 cells / μl in prior 12 months or ≥150 cells / μl at screening and history of exacerbations (≥2 in past 12 months) receiving medium-to-high-dose inhaled corticosteroids. In one embodiment, the antigen binding protein is for use in the treatment of asthma in a patient with type 2 inflammation characterised by an eosinophilic phenotype. In one embodiment, the antigen binding protein is for use in the treatment of asthma in a patient with type 2 inflammationcharacterised by an eosinophilic phenotype on medium- to high-dose inhaledcorticosteroids (ICS). In one embodiment, the antigen binding protein is for use in thetreatment of asthma in a patient with type 2 inflammation characterised by an eosinophilicphenotype on medium- to high-dose inhaled corticosteroids (ICS) plus another asthmacontroller. In one embodiment, the antigen binding protein is for use in the treatment of asthma in adult and pediatric patients aged 12 years and older with type 2 inflammationcharacterised by an eosinophilic phenotype on medium- to high-dose inhaledcorticosteroids (ICS) plus another asthma controller. In one embodiment, the antigenbinding protein is for use in the treatment of asthma in a patient with type 2 inflammationwho are inadequately controlled on medium- to high- dose inhaled corticosteroids (ICS)plus another controller. In one embodiment, the antigen binding protein is for use in the treatment of severe asthma in a patient with type 2 inflammation who are inadequatelycontrolled despite high dose inhaled corticosteroids (ICS) plus another controller. In oneembodiment, the antigen binding protein is for use in the treatment of patients with uncontrolled asthma with type 2 inflammation characterized by blood eosinophil countdespite standard of care with medium- to high-dose inhaled corticosteroids (ICS) plus atleast one additional controller. Further improvements in reducing the annualised rate of exacerbations can beachieved in patients according to blood eosinophil count. Further improvements inreducing the SGRQ score can be achieved in patients according to blood eosinophil count. The patient may prior to treatment, for example at any point in the 12 months prior to treatment, have an absolute blood eosinophil count selected from the group consistingof at least 150 cells / microliter, at least 200 cells / microliter, at least 250 cells / microliter, andat least 300 cells / microliter. The patient may have a peripheral blood eosinophil count of at least 150 cells / microliter. The patient may have a peripheral blood eosinophil count of at least 300 cells / microliter. The patient may have a baseline peripheral blood eosinophil count selected from the group consisting of at least 150 cells / microliter, at least 200 cells / microliter, at least 250 cells / microliter, and at least 300 cells / microliter. The patient may have a baseline peripheral blood eosinophil count of at least 150 cells / microliter. In one embodiment, the patient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter and the annualised rate of exacerbations is reduced by at least 45%, optionally about 50%. In one embodiment, the patient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter and the annualised rate of exacerbations is reduced by at least 50%, optionally about 54%. In one embodiment, the patient has a baseline peripheral bloodeosinophil count of at least 150 cells / microliter and the annualised rate of exacerbations isreduced by at least 55%, optionally about 58%. In one embodiment, the patient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter and the SGRQ score is reduced by at least 4 units, optionally about 4.03 units. In one embodiment, the patient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter andthe SGRQ score is reduced by at least 4 units, optionally about 4.39 units. The patientmay have a baseline peripheral blood eosinophil count of at least 300 cells / microliter. Inone embodiment, the patient has a baseline peripheral blood eosinophil count of at least 300 cells / microliter and the annualised rate of exacerbations is reduced by at least 55%, optionally about 57%. In one embodiment, the patient has a baseline peripheral bloodeosinophil count of at least 300 cells / microliter and the annualised rate of exacerbations isreduced by at least 60%, optionally about 68%. In one embodiment, the patient has abaseline peripheral blood eosinophil count of at least 300 cells / microliter and the SGRQscore is reduced by at least 5 units, optionally about 5.27 units. The annualised rate ofexacerbations may be the annualised rate of clinically significant exacerbations. In one embodiment, the antigen binding protein is for use in a method of reducing the annualised rate of exacerbations in a patient with asthma, wherein the method comprises: a) determining the blood eosinophil count of the patient,b) where the patient has blood eosinophil count of at least 150 cells / microliter orat least 300 cells / microliter, administering to the patient an effective amount of the antigen binding protein. Further improvements in reducing the annualised rate of exacerbations can beachieved in patients according to their asthma symptoms, as measured by ACQ-5. Furtherimprovements in reducing the SGRQ score can be achieved in patients according to theirasthma symptoms, as measured by ACQ-5. The ACQ-5 is a five-item questionnaire,which has been developed as a measure of participants' asthma control that can be quickly and easily completed. The questions are designed to be self-completed by the participant. The 5 questions enquire about the frequency and / or severity of symptoms (nocturnal awakening on waking in the morning, activity limitation, and shortness of breath, wheeze) over the previous week. The response options for all these questions consist of a zero (no impairment / limitation) to six (total impairment / limitation) scale. Higher scores indicate more limitations. Prior to treatment, for example at any point in the 12 months prior to treatment, the patient may have an Asthma Control Questionnaire-5 (ACQ-5) score of at least 1.5 prior to treatment. The patient may have a baseline Asthma Control Questionnaire-5 (ACQ-5) score of at least 1.5. In one embodiment, the patient has a baseline Asthma ControlQuestionnaire-5 (ACQ-5) score of at least 1.5 and the annualised rate of exacerbations isreduced by at least 60%, optionally about 60%. In one embodiment, the patient has a baseline Asthma Control Questionnaire-5 (ACQ-5) score of at least 1.5 and the SGRQ score is reduced by at least 4 units, optionally about 4.12 units. In one embodiment, the patient has a baseline Asthma Control Questionnaire-5 (ACQ-5) score of at least 1.5 and the SGRQ score is reduced by at least 5 units, optionally about 5.1 units. In one embodiment, the antigen binding protein is for use in a method of reducing the annualised rate of exacerbations in patient with asthma, wherein the method comprises:c) determining the baseline ACQ-5 of the patient,d) where the patient has a baseline ACQ-5 of at least 1.5, administering to thepatient an effective amount of the antigen binding protein. Further improvements in reducing the annualised rate of exacerbations can beachieved in patients with comorbid Chronic Rhinosinusitis with Nasal Polyps (CRSwNP).CRSwNP may be reported by patients who have had a co-morbid analysis. The patientmay have past CRSwNP. Past CRSwNP may reflect the situation where some patientshave had their polyps removed surgically and are no longer troubled by them. The patientmay have current CRSwNP. In one embodiment, the patient has comorbid CRSwNP andthe annualised rate of exacerbations is reduced by at least 65%, optionally about 70%. In one embodiment, an effective amount of antigen binding protein is to beadministered to the patient. The effective amount of antigen binding protein may be adose of 100 mg. The antigen binding protein may be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months. In one embodiment, the antigen binding protein is in a pharmaceuticalcomposition. In one embodiment, the pharmaceutical composition comprises the antigenbinding protein in an amount of 100 mg, and a pharmaceutically acceptable excipient. Inone embodiment, the pharmaceutical composition comprises the antigen binding proteinin an amount of 100 mg, and an aqueous liquid formulation at about pH 6.0 comprisingabout 20 mM histidine, about 180 mM trehalose, about 40 mM arginine, about 0.05 mM EDTA and about 0.02% weight of polysorbate 80 to volume. In one embodiment, the patient is human. Further improvements in reducing the annualised rate of exacerbations can beachieved in patients according to region. Further improvements in reducing the SGRQscore can be achieved in patients according to region. In one embodiment, the patient is from China, United State of America or WesternEurope and the annualised rate of exacerbations is reduced by least 60%. In oneembodiment, the patient is from China, United State of America or Western Europe andthe SGRQ score is reduced by least 4 units. In one embodiment, the patient is from China.In one embodiment, the patient is from China and the annualised rate of exacerbations isreduced by at least 80%, optionally about 84%. In one embodiment, the patient is from China and the annualised rate of exacerbations is reduced by at least 80%, optionally about 85%. In one embodiment, the patient is from China and the SGRQ score is reducedby at least 9 units, optionally about 9.6 units. In one embodiment, the patient is biologic-naïve. In one embodiment, the patient is from the United States of America. In one embodiment, the patient is from the United States of America and the annualised rate of exacerbations is reduced by at least 50%, optionally about 55%. In one embodiment, the patient is from the United States of America and the annualised rate of exacerbations is reduced by at least 60%, optionally about 63%. In one embodiment, the patient is from theUnited States of America and the annualised rate of exacerbations is reduced by at least60%, optionally about 64%. In one embodiment, the patient is from the United States ofAmerica and the SGRQ score is reduced by at least 4 units, optionally about 4.51 units. Inone embodiment, the patient is from a Western European country. In one embodiment, the patient is from a Western European country and the annualised rate of exacerbations is reduced by at least 50%, optionally about 53%. In one embodiment, the patient is from a Western European country and the annualised rate of exacerbations is reduced by at least 60%, optionally about 62%. In one embodiment, the patient is from a WesternEuropean country and the annualised rate of exacerbations is reduced by at least 60%,optionally about 66%. In one embodiment, the patient is from a Western European countryand the SGRQ score is reduced by at least 7 units, optionally about 7.58 units. In oneembodiment, the patient is from a Western European country and the SGRQ score is reduced by at least 8 units, optionally about 8.42 units. In one embodiment, the patient is from a Western European country and the SGRQ score is reduced by at least 9 units, optionally about 9.43 units. A Western European country may be Italy, Germany, United Kingdom, Ireland, France, or Spain. A Western European country may be Italy, Germany, United Kingdom, Ireland, France, Hungary or Spain. In embodiment, the patient is from Italy. In one embodiment, the patient is from Germany. In one embodiment, the patient is from United Kingdom. In one embodiment, the patient is from Ireland. In one embodiment,the patient is from France. In one embodiment, the patient is from Hungary. In oneembodiment, the patient is from Spain. In one embodiment, the patient is from Japan. Inone embodiment, the patient is from Japan and the annualized rate of exacerbations is reduced by at least 50%, optionally about 51%. In one embodiment, the patient is fromJapan and the SGRQ score is reduced by at least 8 units, optionally about 8.30 units. Inone embodiment, the patient is of Japanese heritage. In one embodiment, the patient is of Japanese heritage and the annualized rate of exacerbations is reduced by at least 50%, optionally about 51%. In one embodiment, the patient is of Japanese heritage and the SGRQ score is reduced by at least 8 units, optionally about 8.30 units. In one embodiment, the patient is Asian. In one embodiment, the patient is Asian and the patient’s annualised rate of exacerbations is reduced by at least 60%, optionally about 65%. In one embodiment, the patient is Asian and the patient’s annualised rate of exacerbations is reduced by at least 80%, optionally about 84%. In one embodiment, the patient is Asian and the patient’s SGRQ score is reduced by at least 8 units, optionally about 8.41 units. In one embodiment, the patient is Asian and the patient’s SGRQ score isreduced by at least 9 units, optionally about 9.6 units. The Asian patient may be fromChina or Japan. In one embodiment, the patient is of East Asian heritage. In oneembodiment, the patient is of East Asian heritage and the patient’s annualised rate of exacerbations is reduced by at least 60%, optionally about 65%. In one embodiment, thepatient is of East Asian heritage. In one embodiment, the patient is of East Asian heritageand the patient’s annualised rate of exacerbations is reduced by at least 80%, optionally about 84%. In one embodiment, the patient is of East Asian heritage and the patient’s SGRQ score is reduced by at least 8 units, optionally about 8.41 units. In one embodiment, the patient is of East Asian heritage and the patient’s SGRQ score isreduced by at least 9 units, optionally about 9.6 units.In one embodiment, the patient is receiving medium dose inhaled corticosteroids (ICS). In one embodiment, the patient is receiving medium dose ICS and the patient’sannualized rate of exacerbations is reduced by at least 60%, optionally 61%. In oneembodiment, the patient is receiving medium dose ICS and the patient’s annualized rate of clinically significant exacerbations is reduced by at least 60%, optionally 61%. In one embodiment, the patient is receiving medium dose ICS and the patient’s SGRQ score isreduced by at least 5 units, optionally about 5.1 units. The patient may be receivingmedium dose ICS plus another controller. The medium dose ICS may be ≥440micrograms (mcg) Fluticasone propionate (FP) Hydrofluoroalkane (HFA) product daily, orclinically comparable (GINA).In one embodiment, the patient is greater than or equal to (≥)12 years of age. In one embodiment, the patient has a history of ≥2 exacerbations requiring treatment with systemic corticosteroid (CS) (intramuscular [IM], intravenous [IV], or oral), despite the use of medium to high-dose ICS. For patients receiving maintenance CS, the CS treatment for the exacerbations must have been a two-fold dose increase or greater. In one embodiment, the patient is ≥12 years of age and has a pre-bronchodilator FEV1 less than (<) 80% predicted. In one embodiment, the patient is 12-17 years of age and has a pre- bronchodilator FEV1 <90% predicted or FEV1:Forced Vital Capacity (FVC) ratio <0.8. In one embodiment, the patient has a history of regular treatment with medium to high dose ICS (with or without maintenance OCS). The maintenance ICS dose must be >=440 micrograms (mcg) Fluticasone propionate (FP) Hydrofluoroalkane (HFA) product daily, or clinically comparable (GINA). Patients who are treated with medium dose ICS will also need to be treated with LABA. In one embodiment, the patient has an elevated peripheral blood eosinophil count of >=300 cells / microliter in the past 12 months that is related to asthma. In one embodiment, the patient has been on a treatment with at least one additional controller medication, besides ICS, for at least 3 months (for example, LABA, LAMA, leukotriene receptor antagonist [LTRA], or theophylline). In one embodiment, the patient has an elevated peripheral blood eosinophil count of >=300 cells / microliter. In one embodiment, the patient has an elevated peripheral blood eosinophil count of >=150 cells / microliter at that is related to asthma. In one embodiment, the patient has an airway reversibility (FEV1>=12% and 200 milliliters [mL]). In one embodiment, the patient has airway hyperresponsiveness (methacholine: Provocative concentration causing a 20% fall in FEV1 [PC20] of <8 milligrams (mg) / mL, histamine: PD20 of <7.8 micromoles, mannitol: decrease in FEV1 as per the labelled product instructions). Clauses1. An antigen binding protein which binds to human IL-5 comprising a heavy chainvariable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO:10 for use in the treatment of asthma in a patient, wherein the patient’s rate of exacerbations, optionally the patient’s annualised rate of exacerbations, is reduced.2. The antigen binding protein for use according to clause 1, wherein the patient’sannualised rate of exacerbations is reduced by at least, 45%, at least 50% or at least55%.3. The antigen binding protein for use according to clause 1 or clause 2, wherein thepatient’s annualised rate of exacerbations is reduced by at least 60%, at least 65%, atleast 70% or at least 80%.4. The antigen binding protein for use according to clause 1 or clause 2, wherein thepatient’s annualised rate of exacerbations is reduced by at least 48%.5. The antigen binding protein for use according to clause 1 or clause 2, wherein thepatient’s annualised rate of exacerbations is reduced by at least 54%.6. The antigen binding protein for use according to clause 1 or clause 2, wherein thepatient’s annualised rate of exacerbations is reduced by at least 58%.7. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 60%.8. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 63%.9. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 66%.10. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 68%.11. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 71%.12. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 74%.13. The antigen binding protein for use according to any one of clauses 1-3, wherein thepatient’s annualised rate of exacerbations is reduced by at least 85%.14. The antigen binding protein for use according to any one of clauses 1-13, wherein thepatient’s annualised rate of exacerbations is the annualised rate of clinically significantexacerbations, optionally the annualised rate of clinically significant exacerbations over 52 weeks.15. A method of treating asthma comprising administering to a patient an antigen bindingprotein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10, wherein the patient’s rate of exacerbations, optionally the patient’s annualised rate ofexacerbations, is reduced.16. The method of treatment according to clause 15, wherein the patient’s annualised rateof exacerbations is reduced by at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70% or at least 80%.17. The method of treatment of treatment according to clause 15 or 16, wherein thepatient’s annualised rate of exacerbations is the annualised rate of clinically significantexacerbations, optionally the annualised rate of clinically significant exacerbations over 52 weeks.18. An antigen binding protein which binds to human IL-5 comprising a heavy chainvariable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequenceshown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 for use in a method of reducing the rate of exacerbations, optionally the annualised rate of exacerbations, in a patient with asthma.An antigen binding protein for use according to clause 18, wherein the annualisedrate of exacerbations is reduced by at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, or at least 70%.An antigen binding protein for use according to clause 18 or 19, wherein theannualised rate of exacerbations is the annualised rate of clinically significantexacerbations, optionally the annualised rate of clinically significant exacerbations over 52 weeks.A method of reducing asthma exacerbations comprising administering to a patient atherapeutic amount of an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10.The method of method of claim 21, wherein the reduction in asthma exacerbations ismeasured by an annualised rate of exacerbations, wherein the annualised rate ofexacerbations is reduced by at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70% or at least 80%.The method of treatment of treatment according to clause 21 or 22, wherein thepatient’s annualised rate of exacerbations is the annualised rate of clinically significant exacerbations, optionally the annualised rate of clinically significant exacerbations over 52 weeks.An antigen binding protein which binds to human IL-5 comprising a heavy chainvariable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acidsequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO:10 for use in the treatment of asthma in a patient, wherein the patient’s St George'sRespiratory Questionnaire (SGRQ) score is reduced.An antigen binding protein for use according to clause 24, wherein the patient’s SGRQis reduced by at least 4 units, at least 5 units, at least 6 units, at least 7 units, at least 8units or at least 9 units.26. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-25, wherein the heavy chain variable region sequence comprises the amino acid sequence shown in SEQ ID NO: 3; and the light chain variable region sequence comprises the amino acid sequence shown in SEQ ID NO: 4.27. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-26, wherein the antigen binding protein is an antibody.28. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 27, wherein the antibodycomprises an IgG1 Fc domain.29. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 28, wherein the IgG1 Fc domaincomprises a tyrosine residue at position 252, a threonine residue at position 254 and a glutamic acid residue at position 256.30. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-29, wherein the antigen binding protein comprises a heavy chain having the amino acid sequence shown in SEQ ID NO: 1 and a light chain having the amino acid sequence shown in SEQ ID NO: 2.31. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-30, wherein the antigen binding protein is depemokimab.32. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-31, wherein the asthma is mild asthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma, or sub-eosinophilic asthma.33. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 32, wherein the asthma ismoderate eosinophilic asthma or severe eosinophilic asthma.34. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 32, wherein the severe asthma is severe asthma with an eosinophilic phenotype.35. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-31, wherein the asthma is asthma with type 2 inflammation characterised by an eosinophilic phenotype.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according any one of clauses 1-35, wherein the patient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter.The antigen binding protein for use or method of treatment or the method of reducingasthma exacerbations according to any one of clauses 1-36, wherein the patient has a baseline peripheral blood eosinophil count of at least 300 cells / microliter.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein thepatient has a baseline Asthma Control Questionnaire-5 (ACQ-5) of at least 1.5 prior totreatment.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein the patient is from Asia, optionally Japan or China.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein the patient is from United States of America.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein the patient is from a Western European country, optionally Italy, Germany, UnitedKingdom, Ireland, France Hungary or Spain.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35 wherein thepatient is Asian.The antigen binding protein for use or the method of treatment according to clause 42,wherein the patient is of East Asian heritage.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein the patient is biologic naïve.The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein the patient is receiving medium dose inhaled corticosteroids (ICS).The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-35, wherein thepatient has comorbid CRSwNP.47. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 46, wherein the patient has pastor current CRSwNP.48. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-47, wherein an effective amount of antigen binding protein is to be administered to the patient.49. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 48, wherein the antigen bindingprotein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months.50. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to clause 48 or 49, wherein the antigenbinding protein is to be administered to the patient subcutaneously.51. The antigen binding protein for use or method of treatment or the method of reducingasthma exacerbations according to any one of clauses 1-50, wherein the patient is human.52. The antigen binding protein for use or the method of treatment or the method ofreducing asthma exacerbations according to any one of clauses 1-51, wherein the patient is an adult or adolescent (≥12 years).Example 1 – Study Design (SWIFT-1)The study (SWIFT-1) employed a multi-centre, randomised, placebo-controlled,double-blind, parallel group design. The study recruited adults and adolescents (≥12years) with a confirmed diagnosis of severe asthma with an eosinophilic phenotype andwho were on a regimen of medium to high dose inhaled corticosteroids (ICS) (≥440 mcgfluticasone propionate [FP] hydrofluoroalkane product [HFA] daily, or clinically comparable[GINA, 2020]) plus at least one additional controller medication, with evidence ofbronchodilator reversibility or airway hyperresponsiveness as measured bymethacholine / histamine challenge. Eligible participants had uncontrolled asthma with ahistory of repeat exacerbations (≥2 exacerbations in the previous 12 months) while ontheir existing maintenance asthma therapy that excluded any biologics. Participants wererequired to have a blood eosinophil count of ≥150 cells / μL at screening or ≥300 cells / μLdocumented in the 12 months prior to screening. Participants who had received any anti-IL-5 / 5R mAb therapy within the last 12 months were excluded from this study. Participants attended a Pre-screen Visit (Visit 0) to sign consent and a Screening Visit (Visit 1; may be done on the same day as Visit 0) for eligibility assessments. At the conclusion of the run-in period (Visit 2), participants who met the predefined criteria were randomised in a 2:1 ratio to receive either depemokimab 100 mg or placebo, administeredsubcutaneous (SC) (at Week 0 and Week 26) in the clinic via a pre-filled safety syringe(PFS) as an adjunct therapy. Randomisation was stratified based on baseline ICS dose(aiming to up to 50% approximately of participants on medium ICS dose). Participantsremained on their existing stable maintenance asthma therapy throughout the study.The primary outcome measure was the annualised rate of clinically significantexacerbations (i.e. exacerbations requiring systemic corticosteroids (CSs) and / orhospitalisation and / or emergency department (ED) visit) measured over the 52-weektreatment period. Additional efficacy assessment included health-related quality of lifeHRQoL measured with SGRQ.The key inclusion and exclusion criteria used for study participants is listed below. Key inclusion Criteria: ^Adults and adolescents greater than or equal to (>=)12 years of age, at the time ofsigning the informed consent / assent. ^Participants must have a documented physician diagnosis of asthma for >=2 yearsthat meets the National Heart, Lung, and Blood Institute (NHLBI) guidelines or Global Initiative for Asthma (GINA) guidelines and 1. Have, or with high likelihood of having, asthma with an eosinophilicphenotype 2. Have previously confirmed history of >=2 exacerbations requiring treatmentwith systemic corticosteroid (CS) (intramuscular [IM], intravenous [IV], or oral), in the 12 months prior to Visit 1, despite the use of medium to high- dose ICS. For participants receiving maintenance CS, the CS treatment for the exacerbations must have been a two-fold dose increase or greater. ^Persistent airflow obstruction as indicated by:1. For participants >=18 years of age at Visit 1, a pre-bronchodilator FEV1less than (<)80% predicted (The Third National Health and Nutrition Examination Survey [NHANES III]) recorded at Visit 1 2. For participants 12-17 years of age at Visit 1:^ A pre-bronchodilator FEV1 <90% predicted (NHANES III) recordedat Visit 1 OR^ FEV1:Forced Vital Capacity (FVC) ratio <0.8 recorded at Visit 1.^ A well-documented requirement for regular treatment with medium to high doseICS (in the 12 months prior to Visit 1 with or without maintenance OCS). The maintenance ICS dose must be >=440 micrograms (mcg) Fluticasone propionate (FP) Hydrofluoroalkane (HFA) product daily, or clinically comparable (GINA). Participants who are treated with medium dose ICS will also need to be treated with LABA to qualify for inclusion. ^Current treatment with at least one additional controller medication, besides ICS,for at least 3 months (for example [e.g.], LABA, LAMA, leukotriene receptor antagonist [LTRA], or theophylline). Key randomization inclusion criteria: ^For blood eosinophilic count:1. An elevated peripheral blood eosinophil count of >=300 cells / microliter(mcL) demonstrated in the past 12 months prior to Visit 1 that is related to asthma OR 2. An elevated peripheral blood eosinophil count of >=150 cells / mcL atScreening Visit 1 that is related to asthma. ^Evidence of airway reversibility or responsiveness as documented by either:1. Airway reversibility (FEV1>=12% and 200 milliliters [mL]) demonstrated atVisit 1 or Visit 2 using the Maximum Post Bronchodilator Procedure OR 2. Airway reversibility (FEV1>=12% and 200 mL) documented in the 24months prior to Visit 2 (randomization visit) OR 3. Airway hyperresponsiveness (methacholine: Provocative concentrationcausing a 20% fall in FEV1 [PC20] of <8 milligrams (mg) / mL, histamine: PD20 of <7.8 micromoles, mannitol: decrease in FEV1 as per the labelled product instructions) documented in the 24 months prior to Visit 2 (randomization visit). Key exclusion Criteria: ^Presence of a known pre-existing, clinically important lung condition other thanasthma. This includes (but is not limited to) current infection, bronchiectasis, pulmonary fibrosis, bronchopulmonary aspergillosis, or diagnoses of emphysema or chronic bronchitis (chronic obstructive pulmonary disease other than asthma) or a history of lung cancer. ^Participants with other conditions that could lead to elevated eosinophils such ashyper-eosinophilic syndromes including (but not limited to) Eosinophilic Granulomatosis with Polyangiitis (EGPA, formerly known as Churg-Strauss Syndrome) or Eosinophilic Esophagitis. ^A current malignancy or previous history of cancer in remission for less than 12months prior to screening (Participants that had localized carcinoma of the skin which was resected for cure will not be excluded). ^Cirrhosis or current unstable liver or biliary disease per investigator assessmentdefined by the presence of ascites, encephalopathy, coagulopathy, hypoalbuminemia, esophageal or gastric varices, persistent jaundice. ^Participants with current diagnosis of vasculitis. Participants with high clinicalsuspicion of vasculitis at screening will be evaluated and current vasculitis must be excluded prior to enrolment. ^Participants who have received mepolizumab (Nucala), reslizumab(Cinqair / Cinqaero), or benralizumab (Fasenra) within 12 months prior to Visit 1 or who have a previous documented failure with anti-IL-5 / 5 receptor (R) therapy. ^Participants who have received omalizumab (Xolair) or dupilumab (Dupixent)within 130 days prior to Visit. ^Participants who have received any monoclonal antibody (mAb) within 5 half-livesof Visit 1. ^Previously participated in any study with mepolizumab, reslizumab, orbenralizumab and received study intervention (including placebo) within 12 months prior to Visit 1. ^The QT interval corrected using Fridericia's formula (QTcF) >=450 milliseconds(msec) or QTcF >=480 msec for participants with Bundle Branch Block at screening Visit 1. ^Current smokers or former smokers with a smoking history of >=10 pack years(number of pack years = [number of cigarettes per day / 20] times number of years smoked). A former smoker is defined as a participant who quit smoking at least 6 months prior to Visit 1. ^Participants with allergy / intolerance to the excipients of GSK3511294 or a anymAb or biologic. Key randomization exclusion criteria: ^QTcF >=450 msec or QTcF >=480 msec for participants with Bundle BranchBlock, at randomization Visit 2 are excluded. Participants are excluded if an abnormal ECG finding from the 12-lead ECG conducted at Screening Visit 1 is considered to be clinically significant and would impact the participant's participation during the study, based on the evaluation of the Investigator.^ Participants with a clinically significant asthma exacerbation in the 7 days prior torandomization should have their randomization visit delayed until the investigator considers the participant's asthma to be stable. ^Any changes in the dose or regimen of Baseline ICS and / or additional controllermedication (except for treatment of an exacerbation) during the run-in period.Example 2 – Patient characteristics (SWIFT-1)A summary of the patient’s (SWIFT-1) demographic characteristics, asthma history and baseline disease characteristics, and asthma exacerbation history is provided inTables 6, 7 and 8 below.Table 6. Summary of demographic characteristics (SWIFT-1).Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250) Sex n132 250 382F 79 (60%) 144 (58%) 223(58%) M53 (40%) 106 (42%) 159(42%) Age (YEARS) n132 250 382Mean 53.6 54.1 53.9SD 14.91 13.82 14.19Median 56.0 55.5 56.0Min. 15 14 14Max. 78 78 78Age Group (YEARS) n132 250 38212-17 5 (4%) 3 (1%) 8 (2%)18-64 91 (69%) 185 (74%) 276(72%) >=65 36 (27%) 62 (25%) 98 (26%)Ethnicity n132 250 382 Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250)HISPANIC OR LATINO 11 (8%) 12 (5%) 23 (6%)NOT HISPANIC OR LATINO 121 238 (95%) 359(92%) (94%) High Level Racen 132 250 382AMERICAN INDIAN OR ALASKA NATIVE 0 0 0ASIAN 20 (15%) 38 (15%) 58 (15%)BLACK OR AFRICAN AMERICAN 3 (2%) 5 (2%) 8 (2%)NATIVE HAWAIIAN OR OTHER PACIFIC0 0 0ISLANDERWHITE 109 207 (83%) 316(83%) (83%) Race Detailn 132 250 382AMERICAN INDIAN OR ALASKA NATIVE 0 0 0ASIAN - CENTRAL / SOUTH ASIAN HERITAGE 0 0 0ASIAN - JAPANESE HERITAGE 0 0 0ASIAN - EAST ASIAN HERITAGE 20 (15%) 38 (15%) 58 (15%)ASIAN - SOUTH EAST ASIAN HERITAGE 0 0 0BLACK OR AFRICAN AMERICAN 3 (2%) 5 (2%) 8 (2%)NATIVE HAWAIIAN OR OTHER PACIFIC0 0 0ISLANDERWHITE - ARABIC / NORTH AFRICAN HERITAGE 0 0 0WHITE - WHITE / CAUCASIAN / EUROPEAN109207 (83%) 316HERITAGE (83%) (83%) Regionn 132 250 382Europe 85 (64%) 158 (63%) 243(64%)US 18 (14%) 33 (13%) 51 (13%)Rest of World 29 (22%) 59 (24%) 88 (23%)Height (cm)n 132 250 382Mean 167.86 168.08 168.01SD 9.256 9.806 9.608 Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250)Median 168.00 168.00 168.00Min. 142.0 144.2 142.0Max. 188.0 195.6 195.6Weight (kg)n 132 250 382Mean 80.47 78.69 79.31SD 19.871 17.953 18.631Median 77.00 77.40 77.00Min. 51.0 41.1 41.1Max. 154.7 152.8 154.7BMI (kg / m2)n 132 250 382Mean 28.50 27.78 28.03SD 6.472 5.621 5.930Median 27.36 27.30 27.31Min. 18.6 15.1 15.1Max. 53.1 52.6 53.1Table 7. Summary of asthma history and baseline disease characteristics (SWIFT-1).Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250) Duration of Asthma (years)n 132 250 382<1 0 0 0>=1 to <5 15 (11%) 18 (7%) 33 (9%)>=5 to <10 21 (16%) 40 (16%) 61 (16%)>=10 to <15 29 (22%) 43 (17%) 72 (19%)>=15 to <20 16 (12%) 28 (11%) 44 (12%)>=20 to <25 13 (10%) 31 (12%) 44 (12%)>=25 38 (29%) 90 (36%) 128(34%) Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250)Mean 20.0 22.5 21.6SD 16.32 16.14 16.22Median 15.0 18.0 17.0Min. 2 2 2Max. 71 75 75Baseline ICS dose leveln 132 250 382Medium Dose ICS 61 (46%) 118 (47%) 179(47%)High Dose ICS 71 (54%) 132 (53%) 203(53%) Peripheral Blood Eosinophils count related to Asthman 132 250 382>= 300 / µL in the past 12 Months prior to61 (46%) 127 (51%) 188Screening (49%)>= 150 / µL at Screening 123 224 (90%) 347(93%) (91%) Subject intubated in relation to their asthma prior to the studyn 132 250 382Yes 2 (2%) 9 (4%) 11 (3%)No 130 241 (96%) 371(98%) (97%) Maintenance OCS at baselinen 132 250 382Yes 13 (10%) 8 (3%) 21 (5%)No 119 242 (97%) 361(90%) (95%) Baseline OCS daily dose (prednisone equivalent)n 13 8 21<7.5 mg / day 8 (62%) 5 (63%) 13 (62%)>=7.5 - <15 mg / day 2 (15%) 3 (38%) 5 (24%)>=15 - <30 mg / day 3 (23%) 0 3 (14%)>= 30 mg / day 0 0 0 Placebo Depemokimab 100 mg Total (N=132) SC (N=382) (N=250)Mean 8.46 6.88 7.86SD 5.158 2.588 4.351Median 5.00 5.00 5.00Min. 5.0 5.0 5.0Max. 20.0 10.0 20.0Total IgE (U / mL)n 130 250 380Geo. Mean 180.41 144.38 155.82SD Logs 1.520 1.525 1.525Median 191.05 180.60 184.75Min. 1.9 1.9 1.9Max. 5265.6 12142.8 12142.8Table 8. Summary of asthma exacerbation history (SWIFT-1).Placebo Depemokimab 100 Total (N=132) mg SC (N=382) (N=250) Number of exacerbations that required oral / systemic corticosteroid in past 12 monthsn 132 250 3820 0 1 (<1%) 1 (<1%)1 0 0 02 118 210 (84%) 328(89%) (86%)3 9 (7%) 32 (13%) 41 (11%)4 3 (2%) 2 (<1%) 5 (1%)>4 2 (2%) 5 (2%) 7 (2%)Number of exacerbations requiring intubation in past 12 monthsn 2 9 110 0 4 (44%) 4 (36%)1 0 1 (11%) 1 (9%)2 2 (100%) 4 (44%) 6 (55%)3 0 0 0 Placebo Depemokimab 100 Total (N=132) mg SC (N=382) (N=250) >4 0 0 0Number of exacerbations that required hospitalization in past 12 months n132 250 3820 125 233 (93%) 358(95%) (94%) 14 (3%) 13 (5%) 17 (4%)2 3 (2%) 4 (2%) 7 (2%)3 0 0 04 0 0 0>4 0 0 0Previous causes of exacerbation [1] n132 250 382Air pollution 36 (27%) 72 (29%) 108(28%) Allergy 52 (39%) 108 (43%) 160(42%) Aspirin 2 (2%) 10 (4%) 12 (3%)Other NSAIDS 2 (2%) 4 (2%) 6 (2%)Cold Air / Cold Weather 49 (37%) 87 (35%) 136(36%) Exercise 41 (31%) 81 (32%) 122(32%) Stress / Emotions 26 (20%) 59 (24%) 85 (22%)Tobacco Smoke 17 (13%) 31 (12%) 48 (13%)Withholding or Reducing Asthma Medication 25 (19%) 42 (17%) 67 (18%)Common cold 56 (42%) 98 (39%) 154(40%) Upper respiratory infection other than common cold 48 (36%) 84 (34%) 132(35%) Lower respiratory infection 41 (31%) 79 (32%) 120(31%) Other 17 (13%) 44 (18%) 61 (16%)Example 3 – Summary of Results (SWIFT-1) This study (SWIFT-1) demonstrated that depemokimab reduced exacerbations inpatients with asthma with an eosinophilic phenotype. Overall, the annualised rate ofclinically significant exacerbations over 52 weeks was significantly lower in patientstreated with depemokimab compared with placebo. The annualised rate of clinicallysignificant exacerbations over 52 weeks was reduced by 58% in patients treated withdepemokimab compared with placebo (p<0.001).This study also demonstrated that depemokimab reduced exacerbations, in particular, in patients with a baseline blood eosinophil count of at least 150 or 300 cells / µL. This study also demonstrated that patients may be stratified by ACQ-5 and region to achieve improved reduction of annualised rate of clinically significantexacerbations over 52 weeks and greater change from baseline in Saint (St.) George'sRespiratory Questionnaire (SGRQ) total score at Week 52. For example, a percentagereduction in exacerbation rate with depemokimab of 85% in the China subpopulation ofSWIFT-1 was demonstrated, which may be explained by the pool of patients with severeasthma being relatively biologic-naïve (Chen et al., ERJ Open Res. 2024 May; 10(3):00750-2023). The effects of depemokimab on annualised rate of clinically significant exacerbations over 52 weeks and on change from baseline in Saint (St.) George'sRespiratory Questionnaire (SGRQ) total score at Week 52, across different subgroups, issummarised in Table 9.

[0003] ;te r et) )Ssil4 7it 31.gsno% 0r1 / 0 70-yr inlyu 0 o 3ci1 % 8 8,2. ,7 danCli≥ m7 / 6 %5-3s.ota ulll=9 n4(01ircAlhlp e -(o cpsxeuFnie ,n(so rRopE et)’s itnu eil6 ) 5 e no1 %3.greoril00rc1 / % 5 5 4 ovrg ei1 b s 361 6,1.1,4 eetu a < m 4 -6S B / sll=%.n1(6Gine -(.t yycSdb= uterrocetQsS til8 ) ) 9 0 Rf%3Goln 0ou 5r1 / 1.Seato 1ci51 % 7 9 3.0- ; sm oC 185, ,o %4- 7 dl dT li≥ / h sll=94n3.(8r-(o e w nQ p e coR oftGnisSo rose dEta ) )ts ln eil2 % 3 eea nil0o 534.Rt5rc / 7 % 8 7 01 =asein s 1 a < m15,59.0,0 W deoitB / s=% lln 225.o - Riva e(8-(ebc;recp erec)ax1- a n a 8,),9 )oro ini= 3 / h % % 74.6 u E TtFh h I C C n 0 5 7 % 2 86(35.9 99- 13.Ew-(0 =st44n U E na WicS, li;afipW 9,) % 9 3 2.)4 aicn o= 5 / %5 0 %igR n 92 75(74.4 86- 12.v-1rterS( ta npyl3,) 7,)iedeaicS U= 3n / % 8 8 3 % %5.- 766(64.4c i- (46.nznli1 8 1 5 e n d moCoiifdfgoenr7,- ) 8,n n 4 ) RetU= 8 / % % %5.0.1ocaretse E n 8 66 0 17a 44(8 - 41.1- 1 (=IllC aRW; sedin, ,)5- dezrle1 ) t U= 7 / % % 7 4 8 e u 7 %8. ir lca s E n 71- 9 89.3 27.0 au a 3 -(4 -(1 ninn E n s)nA 9, io etS ),)tsatAf5-5.7 =1% % 9 0 8 3 1 eF(o Q 1 n / 1 0 0 %3. .98.uStsCi≥ 0 64(75-sA -(0- Qdeslyeer1 n ole c oitsailSi54,),9 )rtn Usn es.= 6 / % % % 42.7 nlyA a1n 8 35186.1 65.o = a.B < 2(7 - 9 S n9(Ca U alles;n melubatoimlhirt ni etornat :tsafln e T y n l a a:eg n af iot2teA h acibr2 sat ioRl)Ie e n nT a 5ecn)I= n io Tcifie 5 n crk netcaCgiu nle QerkmterC 5in -tls:sCgia e e v ecrud n %5 a s R o ee a eefS x E O W e P e R n A9(h a G c C B S S WrTif%5 QeeD9(C uto A Q N 5for,) lerein aie.o b ap mwfQR b m S olo a niosGS,ecu, inlan ebich n h p wetu a ep- / c ioneptcnirnli org ba obar vitaro g uitavesatmeFc ,ag o dle eau o nicb ekolad e nn g re po h,itpumtmpla a ,)gpa e n e +atworerpo rIg in4,n S e Ale gte bydst ,3c Fdubsn K m a, re e os taip Uui, ss2 h m ( P,cy .tsnisidtrn a alyrp ni er iov,et. a eotustusg e pfmrdois or rer lau a g na alolcinh o erG mhte acsae, rn nipa omicl cCblyeiteictrd hpat sinii amtaetarot ecd matuI(n l brae p ae g Qn nsdeecrtne elli p o e e RrGe orsa a zdli ax yb der gfn ,)Sif ed eareynifeen,)ptcag + e dterh u ud ni4i,nlne elae e p dgig org nseu3saim wossh iarbuocd,bte 2ya h dse gip no ssa( emrporyrb wurismdTn uuiun w oot it .toitod a, sisfr irEdsis ise e 1lglaye ph v,tivup54bnrmrm(VE anernois yo u es tso efresF ao o d ec itivbs a,pp1 u S e eethlbrVoA ht Wpdn.sSict,atecErgFei)c n C d e a inot axFdtn hst lio n bitIra e p h Qe etetn a upbinl tC R nrG,) ic mtiiperic e esecoSh igd e aestnt Rca a F ber .nihrprtarahc xp e,pr tr% eony ipfez tp 0bicn uot0inlmecptro Cr ,.)aorail1es iure u a p e diaicifgtd*)a d porn b n mla sso obergiu n nitm b d u o RigehcarmootNP( ,sr(lause amtn oetf es itd dc.est in yllara eba e o o n u a di.ahic rt -er- gnd hc ,nsyb d a e C, infor1(a SC n pocd m nifalc speshcI oru osutiske d o d afn o e m.s s setainlafeb- rg a w e d o es inler t sn eio psiaieC( sir s tily avalaseslpniya e eslyelypsa o b,ul. a bn mta mdanorancpcaa n,pliea norn a u dad u nc in ause artaf ocEe p n ua or sih puorbyeststonrifon gbe C og,htna nh- e erg outnirgterb,aipaicitpstosd asbit sard b n o pu i u u,nle aeucsoinhtr icatrP:]E:]WS:ib]rt ioullnorS: mtal ra g C brp a p1[2[o R3[ isg dern a n]e4[erttotuso F 501 51 02Example 4 – Patient characteristics (SWIFT-2)A further study (SWIFT-2) was conducted. SWIFT-1 and SWIFT-2 were replicate 52-week, randomized, double-blind placebo-controlled, parallel-group, multi-centre phase III clinical trials. Both trials assessed the efficacy and safety of depemokimab adjunctive therapyin patients with asthma who were randomized to receive depemokimab or placebo, in additionto their standard of care treatment with medium to high-dose inhaled corticosteroids plus atleast one additional controller. A summary of the patient’s (SWIFT-2) demographiccharacteristics, asthma history and baseline disease characteristics, and asthma exacerbation history is provided in Tables 10, 11 and 12 below. Table 10. Summary of demographic characteristics (SWIFT-2).Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252) Sex n128 252 380F 81 (63%) 160 (63%) 241(63%) M47 (37%) 92 (37%) 139(37%) Age (YEARS) [1] n128 252 380Mean 51.2 53.6 52.8SD 16.58 16.00 16.22Median 53.0 57.0 55.5Min. 12 12 12Max. 81 82 82Age Group (YEARS) [1] n128 252 38012-17 10 (8%) 12 (5%) 22 (6%)18-64 93 (73%) 169 (67%) 262(69%) >=65 25 (20%) 71 (28%) 96 (25%)Ethnicity n128 252 380 Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252)HISPANIC OR LATINO 20 (16%) 45 (18%) 65 (17%)NOT HISPANIC OR LATINO 108 207 (82%) 315(84%) (83%) High Level Racen 128 252 380AMERICAN INDIAN OR ALASKA NATIVE 1 (<1%) 2 (<1%) 3 (<1%)ASIAN 23 (18%) 52 (21%) 75 (20%)BLACK OR AFRICAN AMERICAN 11 (9%) 17 (7%) 28 (7%)NATIVE HAWAIIAN OR OTHER PACIFIC0 0 0ISLANDERWHITE 91 (71%) 181 (72%) 272(72%)MIXED RACE 2 (2%) 0 2 (<1%)Race Detailn 128 252 380AMERICAN INDIAN OR ALASKA NATIVE 1 (<1%) 2 (<1%) 3 (<1%)ASIAN - CENTRAL / SOUTH ASIAN HERITAGE 0 2 (<1%) 2 (<1%)ASIAN - JAPANESE HERITAGE 18 (14%) 41 (16%) 59 (16%)ASIAN - EAST ASIAN HERITAGE 5 (4%) 8 (3%) 13 (3%)ASIAN - SOUTH EAST ASIAN HERITAGE 0 1 (<1%) 1 (<1%)BLACK OR AFRICAN AMERICAN 11 (9%) 17 (7%) 28 (7%)NATIVE HAWAIIAN OR OTHER PACIFIC0 0 0ISLANDERWHITE - ARABIC / NORTH AFRICAN HERITAGE 0 3 (1%) 3 (<1%)WHITE - WHITE / CAUCASIAN / EUROPEAN 91 (71%) 178 (71%) 269HERITAGE (71%)MIXED RACE 2 (2%) 0 2 (<1%)Regionn 128 252 380Europe 57 (45%) 108 (43%) 165(43%)US 46 (36%) 90 (36%) 136(36%) Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252)Rest of World 25 (20%) 54 (21%) 79 (21%)Height (cm)n 128 252 380Mean 165.92 165.98 165.96SD 9.473 10.112 9.889Median 165.00 165.00 165.00Min. 143.0 143.7 143.0Max. 191.0 191.0 191.0Weight (kg)n 128 252 380Mean 79.06 79.83 79.57SD 19.472 21.132 20.565Median 77.75 76.00 76.30Min. 37.7 34.6 34.6Max. 139.6 161.0 161.0BMI (kg / m2)n 128 252 380Mean 28.70 28.74 28.73SD 6.729 6.100 6.310Median 28.36 27.90 28.03Min. 16.4 14.2 14.2Max. 56.6 48.8 56.6Table 11. Summary of asthma history and baseline disease characteristics (SWIFT-2).Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252) Duration of Asthma (years)n 128 252 380<1 0 0 0>=1 to <5 13 (10%) 23 (9%) 36 (9%) Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252)>=5 to <10 17 (13%) 35 (14%) 52 (14%)>=10 to <15 22 (17%) 42 (17%) 64 (17%)>=15 to <20 13 (10%) 20 (8%) 33 (9%)>=20 to <25 14 (11%) 24 (10%) 38 (10%)>=25 49 (38%) 108 (43%) 157(41%)Mean 24.1 25.6 25.1SD 17.93 18.73 18.46Median 19.0 21.0 20.0Min. 2 2 2Max. 78 73 78Baseline ICS dose leveln 128 252 380Medium Dose ICS 60 (47%) 94 (37%) 154(41%)High Dose ICS 68 (53%) 158 (63%) 226(59%) Peripheral Blood Eosinophils count related to Asthman 128 252 380>= 300 / uL in the past 12 Months prior to Screening 66 (52%) 151 (60%) 217(57%)>= 150 / uL at Screening 118 219 (87%) 337(92%) (89%) Subject intubated in relation to their asthma prior to the studyn 128 252 380Yes 5 (4%) 6 (2%) 11 (3%)No 123 246 (98%) 369(96%) (97%) Maintenance OCS at baselinen 128 252 380 Placebo Depemokimab 100 mg Total (N=128) SC (N=380) (N=252)Yes 6 (5%) 13 (5%) 19 (5%)No 122 239 (95%) 361(95%) (95%) Baseline OCS daily dose (prednisone equivalent)n 6 13 19<7.5 mg / day 3 (50%) 9 (69%) 12 (63%)>=7.5 - <15 mg / day 3 (50%) 4 (31%) 7 (37%)>=15 - <30 mg / day 0 0 0>= 30 mg / day 0 0 0Mean 6.67 5.73 6.03SD 3.028 2.826 2.841Median 6.25 5.00 5.00Min. 2.5 2.0 2.0Max. 10.0 10.0 10.0Total IgE (U / mL)n 128 246 374Geo. Mean 189.25 158.29 168.27SD Logs 1.413 1.460 1.444Median 200.00 167.00 180.10Min. 2.2 4.8 2.2Max. 2702.4 16198.6 16198.6Table 12. Summary of asthma exacerbation history (SWIFT-2).Placebo Depemokimab 100 Total (N=128) mg SC (N=380) (N=252) Number of exacerbations that required oral / systemic corticosteroid in past 12 monthsn 128 252 3800 0 0 01 0 0 0 Placebo Depemokimab 100 Total (N=128) mg SC (N=380) (N=252)2 90 (70%) 188 (75%) 278(73%)3 17 (13%) 36 (14%) 53 (14%)4 7 (5%) 14 (6%) 21 (6%)>4 14 (11%) 14 (6%) 28 (7%)Number of exacerbations requiring intubation in past 12 monthsn 5 6 110 5 (100%) 6 (100%) 11(100%)1 0 0 02 0 0 03 0 0 04 0 0 0>4 0 0 0Number of exacerbations that required hospitalization in past 12 monthsn 128 252 3800 111 233 (92%) 344(87%) (91%)1 12 (9%) 6 (2%) 18 (5%)2 2 (2%) 10 (4%) 12 (3%)3 0 2 (<1%) 2 (<1%)4 0 0 0>4 3 (2%) 1 (<1%) 4 (1%)Previous causes of exacerbation [1]n 128 252 380Air pollution 55 (43%) 110 (44%) 165(43%)Allergy 62 (48%) 120 (48%) 182(48%)Aspirin 5 (4%) 6 (2%) 11 (3%)Other NSAIDS 4 (3%) 5 (2%) 9 (2%) Placebo Depemokimab 100 Total (N=128) mg SC (N=380) (N=252) Cold Air / Cold Weather 51 (40%) 95 (38%) 146(38%) Exercise 49 (38%) 79 (31%) 128(34%) Stress / Emotions 33 (26%) 75 (30%) 108(28%) Tobacco Smoke 29 (23%) 60 (24%) 89 (23%)Withholding or Reducing Asthma Medication 32 (25%) 54 (21%) 86 (23%)Common cold 68 (53%) 124 (49%) 192(51%) Upper respiratory infection other than common cold 73 (57%) 138 (55%) 211(56%) Lower respiratory infection 48 (38%) 81 (32%) 129(34%) Other 23 (18%) 28 (11%) 51 (13%)Example 5 – Summary of Results (SWIFT-2)The SWIFT-2 study demonstrated that depemokimab reduced exacerbations in patient’s with asthma with an eosinophilic phenotype. Overall, the annualised rate of clinically significant exacerbations over 52 weeks was significantly lower in patients treated with depemokimab compared with placebo. The annualised rate of clinically significant exacerbations over 52 weeks was reduced by 48% in patients treated with depemokimab compared with placebo (p<0.001). The effects of depemokimab on annualised rate of clinically significant exacerbations over 52 weeks and on change from baseline in Saint (St.) George's Respiratory Questionnaire (SGRQ) total score at Week 52, across different subgroups, is summarised in Table 13.srisetlytil7 ) ) a n 4 % 0 0or159.g u / 6 4 2yn o 0 3ci9 %5,8. , r in8odAllCli≥ m6 / 4 %1-5. ta ulcu h sll=4 n1(6-ir xF p(o eps e(pnc i e , s u o rRnorE etg eil5 ) )’soitn nor0 % 3 e 49.grebiul0 e 0 S s 3ci1 / 9 % 7 9 2 ovrm555,2.2,-0 eetya B < / %5s=2.n 7Ginb ll2(-(.t yeercSd = uocrtSletQsi 3 ) )f4 Roattlno1o u 0 5r2c / %52.GSeToi3 % 6 3 0 C 1 1,5. , ; so ≥ m105 %3- 0Qli / 3dl dh sll=7.2 7-ro eR G po e n( (w n oS nc iftd so rotssanaE et) )0leseil9 % nor3 / 67.eRtnil0 7 e 5ci5 %,2 31 =aoits 1 m182 %1.4,6 W dea a B < / s=7 n 141.o 5 Rivbrll- -( ;eeec) c(eceax2-EtT na na 1,),p 9 )orronFIp= 4 / h % % 0 %3a a p.3.9 u J a n 8 1 7 8 77.EwJ 1 5 -(78- 1i- 0 =scW S(Ut3n5if ;t ,El;anige W 4,) 3 3 3 )iSS o= 5 / %6 % %8. .2 ap53. icyR n 52 4 6-l(277- 1l-(0-vrtertaa npic, ,idein0 )lS U= 9% 2 4 ) n / 6 9 %87%20. .8ec iz1 48.n Cf4 4(7 -(6 e mon d o oifdeitg a enr- , ),n ReRt2 3 5 )on a s U= 5 / %4 11c rl e E n 8 3 % 2 53% ( 8. .79- 77.1=I lad 1- C e W( ; szile ,5- daunrne6 ),) e u t U= 5 / % % 6 6 2.8ir lcn s A a E n 9 5 0 % 4 2 48.7 3 39.ainfE 2 -(-(01 nn s)oio etSsi 5-sQ5.4, ,t1=8 ) 1 / %7 % 1 8 ) 1 %40.0.7seatA 70.uS F(tlyC ≥ n 5 42(63- -(1 QdeaA er9lesn e o A nilc S oitsi53,) 7,2 )rtn Us.e.3 sa1 = 6n / % 0 5 % %3.4.9 nly53(9076.o = a1B < 3 7 - -(6 S nlCea U alba s;T n melu t oimlhirt ni etornat :tsafln e y n l a a:eg n af iot2teA h acibr2 5 sat ioRl)Ie e n nT a 5ecn)I= n io Tcifie n crk netcaCgiu nle QerkmterC 5in -tls:sCgia e e v ecrud n %5 a s R o ee a eefS x E O W e P e R n A9(h a G c C B S S WrTif%5 QeeD9(C uto A Q N 5fde o nlere.rife eiafQ ob bdm i olwo R a niohsGeS, cmsuinnW bicp h nw ete ulap- / oepiotoRvacn a oirnli org ba b, it rg uitavesatme)a dlc iang o e u o nicb ekolaa e erp pn ge o h,itpmtmpS na ,)gpu a eo,e +atS wore c g irp n 4,ne Ale gte bydstn 3c Fdubsnaarm, re os taipF uic,ss2 e h m ( P,try.tsnisid r a aleyrp ni eor iov,et. t ustusg eer lau n a g dornr lca p n oisg a alo pfuhe acsaca orH mte, rn nipiclJa o eictblyeit rmd hsn pati iamtaetarot ecd matIi(n l bra p a e e g Qnellunsdeecrtnip o e e Rereorsa a zdli aax yd re ber gGfn ta ,)Sife ded e,pcg +tereynifen)h u uinlae eod ni4ln e e p dgigrg nsu,3eswa oissh iarboucd,bmth e 2 a dse gip no ssa(myporeyrwrbn urismdn w o uuiu od asisfr t it T.to iisis is tlaorEde e,1lgye ph v,tivu45bnrmu es trm(VE anernois ypo s of esF aoitiv,bppS e ere o d e e tcht sa lbr1 u A ht Wp n.sdSic,ateV c EorgFei)c n C d e na ot axFdtn hsit lo bitIerp p a Qe etetn na u aibinl tnJpperic R ecerR G,) ic mtisecoSh isgd aetn a a F ber .neihrprtatrhxpr t y ipacp e, r% eonicfez tp 0 n uot0inlbme ptro Cr ,aorail1ee dicifgtd*) saiu cre u a pbde porg n b n la .)n n o o hit rimmotb d mu o naigNP(. iseca nr oyr(lausetlmtoretf es id dcueswtala a ebis.a- a d Tic rterre - g o o n nda dn Shc ,oyba e,nind m nifalfop 1(a C n pucspcf seshcI ororautikeaoet inlafo eb- g wso.dJ, sa d ie eit snler t se msn eisiais r saisespneisopse dly avblaelyp a a o,ullya c . a b ely,nli mta mordanorna ncpana n pea n eafn a u Cad ustocp nocpausarte oE,uargsia puorbyhtnstna nh- rai elarorn b g ou etJ org, ,snigterbp nipa itpstosatsbitu u u,ard b ne o u a nlaellucsorpictr icatrP:]E:]A(S:ib]rt iounorS: mtala gaJbrp a p1[2[ sa3[ isg dern a n]e4[erttotuso F 501 51 02Example 6 – Summary of Results (SWIFT-1 and SWIFT-2)The SWIFT-1 and SWIFT-2 studies (pooled data) demonstrated that depemokimab reduced exacerbations in patients with asthma with an eosinophilic phenotype. Overall, the annualised rate of clinically significant exacerbations over 52 weeks was significantly lower inpatients treated with depemokimab compared with placebo. The annualised rate of clinicallysignificant exacerbations over 52 weeks was reduced by 54% in patients treated with depemokimab compared with placebo. There was also a 72% reduction in the annualised rate of exacerbations requiringhospitalisations and / or emergency department (ED) visits with depemokimab vs placebo (pooledanalysis; rate ratio 0.28 [95% CI: 0.13, 0.61; p=0.002]). Furthermore, analysis of time to first exacerbation demonstrated a probability of having an exacerbation event over the 52-week study (95% CI) of 32% (27%, 38%) in SWIFT-1, 33% (27%, 39%) in SWIFT-2 and 32% (28%, 37%) in the pooled analysis with depemokimab and 47% (39%, 56%), 51% (42%, 60%), and 49% (43%, 55%), respectively, with placebo (hazard ratio [95% CI]; SWIFT-1: 0.56 [0.40, 0.79]; SWIFT-2: 0.53 [0.38, 0.74]; pooled: 0.54 [0.43, 0.69]). These pooled data also demonstrated that patients with a baseline blood eosinophil countof at least 150 or 300 cells / µL, patients from certain regions such as Western Europe, US, Rest of the World (RoW), and patients with a medium baseline ICS dose may achieve improved reduction of annualised rate of clinically significant exacerbations over 52 weeks and greater change from baseline in Saint (St.) George's Respiratory Questionnaire (SGRQ) total score at Week 52. The pooled data from SWIFT-1 and SWIFT-2 studies demonstrating the effects of depemokimab on annualised rate of clinically significant exacerbations over 52 weeks and on change from baseline in Saint (St.) George's Respiratory Questionnaire (SGRQ) total score at Week 52, across different subgroups, is summarised in Table 14. Depemokimab efficacy in reducing annualised exacerbation rate in the CRSwNP subpopulation from SWIFT-1 / 2 was also evaluated. Annualised exacerbation rate was analysed in patients with past or current CRSwNP at baseline at Week 52. At Week 52, among CRSwNP subpopulation, the annualised exacerbation rates were 0.51 (95% confidence interval [CI]: 0.33, 0.77; n=80) for depemokimab and 1.70 (95% CI: 1.02, 2.82; n=33) for placebo, with the depemokimab versus placebo rate ratio of 0.30 (95% CI: 0.15, 0.58; p<0.001). The exacerbation rate was reduced by 70% (95% CI: 42%, 85%) comparedwith a 54% reduction observed in the overall population of the SWIFT-1 / 2 studies. Twice-yearly depemokimab, compared with placebo, reduced clinically significant asthmaexacerbations in patients with type 2 asthma and comorbid CRSwNP. This reduction wasgreater than the exacerbation rate reduction observed in the overall asthma population of the SWIFT-1 / 2 studies.

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Claims

1. CLAIMS1. An antigen binding protein which binds to human IL-5 comprising a heavy chainvariable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having theCDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 for use in the treatment of asthma in a patient, wherein the patient’s rate of exacerbations is reduced.

2. The antigen binding protein for use according to claim 1, wherein the patient’s rate ofexacerbations is an annualised rate of exacerbations, wherein the annualised rate of exacerbations is reduced by at least 45%, at least 50%, at least 55%, at least 60%, atleast 65%, at least 70% or at least 80%.

3. An antigen binding protein which binds to human IL-5 comprising a heavy chainvariable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having theCDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10 for use in the treatment of asthma in a patient, wherein the patient’sSGRQ score is reduced.

4. An antigen binding protein for use according to claim 3, wherein the patient’s SGRQscore is reduced by at least 4 units, at least 5 units, at least 6 units, at least 7 units, atleast 8 units or at least 9 units.

5. The antigen binding protein for use according to any one of claims 1-4, wherein theheavy chain variable region sequence comprises the amino acid sequence shown in SEQ ID NO: 3; and the light chain variable region sequence comprises the amino acid sequence shown in SEQ ID NO: 4.

6. The antigen binding protein for use according to any one of claims 1-5, wherein theantigen binding protein is an antibody.

7. The antigen binding protein for use according to claim 6, wherein the antibodycomprises an IgG1 Fc domain.

8. The antigen binding protein for use according to claim 7, wherein the IgG1 Fc domaincomprises a tyrosine residue at position 252, a threonine residue at position 254 and a glutamic acid residue at position 256.

9. The antigen binding protein for use according to any one of claims 1-8, wherein theantigen binding protein comprises a heavy chain having the amino acid sequence shown in SEQ ID NO: 1 and a light chain having the amino acid sequence shown in SEQ ID NO: 2.

10. The antigen binding protein for use according to any one of claims 1-9, wherein theantigen binding protein is depemokimab.

11. The antigen binding protein for use according any one of claims 1-10, wherein theasthma is mild asthma, moderate asthma, severe asthma, mild eosinophilic asthma, moderate eosinophilic asthma, severe eosinophilic asthma, uncontrolled eosinophilic asthma, eosinophilic asthma, or sub-eosinophilic asthma.

12. The antigen binding protein for use according to claim 11, wherein the asthma ismoderate eosinophilic asthma or severe eosinophilic asthma.

13. The antigen binding protein for use according any one of claims 1-12, wherein thepatient has a baseline peripheral blood eosinophil count of at least 150 cells / microliter.

14. The antigen binding protein for use according to any one of claims 1-13, wherein thepatient has a baseline peripheral blood eosinophil count of at least 300 cells / microliter.

15. The antigen binding protein for use according to any one of claims 1-12, wherein thepatient has a baseline Asthma Control Questionnaire-5 (ACQ-5) score of at least 1.5.

16. The antigen binding protein for use according to any one of claims 1-12, wherein thepatient is from Asia, optionally China or Japan.

17. The antigen binding protein for use according to any one of claims 1-12, wherein thepatient is from the United States of America.

18. The antigen binding protein for use according to any one of claims 1-12, wherein thepatient is from a Western European country, optionally Italy, Germany, United Kingdom, Ireland, France, Hungary or Spain.

19. The antigen binding protein for use according to any one of claims 1-12, wherein thepatient is receiving medium-dose inhaled corticosteroids (ICS).

20. The antigen binding protein for use according to any one of claims 1-19, wherein aneffective amount of antigen binding protein is to be administered to the patient.

21. The antigen binding protein for use according to claim 20, wherein the antigen bindingprotein is to be administered to the patient at a dose of 100 mg once every 26 weeks or once every 6 months.

22. A method of reducing asthma exacerbations comprising administering to a patient atherapeutic amount of an antigen binding protein which binds to human IL-5 comprising a heavy chain variable region having the CDRH1 amino acid sequence shown in SEQ ID NO: 5, the CDRH2 amino acid sequence shown in SEQ ID NO: 6, and the CDRH3 amino acid sequence shown in SEQ ID NO: 7; and a light chain variable region having the CDRL1 amino acid sequence shown in SEQ ID NO: 8, the CDRL2 amino acid sequence shown in SEQ ID NO: 9, and the CDRL3 amino acid sequence shown in SEQ ID NO: 10.

23. The method of claim 22, wherein the reduction in asthma exacerbations is measuredby an annualised rate of exacerbations, wherein the annualised rate of exacerbations is reduced by at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70% or at least 80%.