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Regulatory T cell (Treg) immunomodulatory function significantly compromised and inflammatory cytokines and chemokines significantly increased in FTD patients COYA 302, Coya’s lead investigational product, is believed to restore Treg immunomodulatory function and target the inflammatory milieu observed in neurodegenerative diseases like FTD HOUSTON--(BUSINESS WIRE)-- Coya Therapeutics, Inc. (“Coya” or the “Company”), a clinical-stage biotechnology company developing biologics primarily focused on the restoration of regulatory T cell (Treg) immunomodulatory function, announces the presentation of data demonstrating the role of the peripheral immune system in the pathophysiology of Frontotemporal Dementia (FTD) from a biomarker study conducted at the Houston Methodist Hospital by Dr. Stanley Appel and Dr. Alireza Faridar and funded by the Houston Methodist Clinical Scholar Award Program. The poster presentation was shared for the first time today at the AD/PD 2024 Conference in Lisbon, Portugal and can be found here. The poster is titled, “Deciphering the Role of the Peripheral Immune System in the Pathology of Frontotemporal Dementia.” “The data from this biomarker study clearly depicts a compromised peripheral immune environment present in patients with FTD that, we believe, contributes to the pathophysiology of the disease process. Further, we believe that targeting systemic inflammation with COYA 302 may lower both peripheral and central nervous system inflammatory cell types while enhancing Treg function and may be a meaningful approach for FTD. We intend to Investigational New Drug (IND) application with the FDA for COYA 302 in FTD later this year and initiate a Ph. 2 trial in FTD patients shortly thereafter,” stated Fred Grossman, Chief Medical Officer at Coya Therapeutics. Summary of Study Results The study was designed to evaluate Treg immunosuppressive function, monocyte mRNA expression, levels of inflammatory cytokines and chemokines, and immune cell markers in peripheral blood mononuclear cells (PBMCs) in blood samples of 22 FTD patients and 11 age-matched healthy individuals as a control group. Treg Function Compromised: Treg suppressive function was significantly reduced in FTD, compared to controls (p<0.01), demonstrating that Treg immunomodulatory function is negatively impacted in FTD. Pro-Inflammatory Systemic Immune Activity: Plasma levels of inflammatory chemokines and cytokines, including C-X-C motif chemokine ligand 9 (CXCL9), CXCL10, CXCL11, CXCL12, tumor necrosis factor alpha (TNFα), chemokine (C-C motif) ligand 3 (CCL3), CCL7, and colony stimulating factor 1 (CSF-1) were consistently and significantly increased in FTD patients (p<0.05). In addition, several inflammation transcripts in monocyte genes known to be involved in neuroinflammatory signaling pathways were dysregulated in FTD, compared to controls. Results of the study demonstrate that FTD patients exhibit a compromised immunosuppressive function of Tregs, along with increased peripheral levels of inflammatory cytokines and chemokines, dysregulation of peripheral monocyte’s inflammation transcriptome and systemic activation of the inflammatory cascade, supporting the critical role of the immune system in the pathophysiology of FTD. The data in FTD is consistent the Treg dysfunction and increased levels of inflammatory cytokines and chemokines previously reported by Coya in other serious and progressive neurodegenerative diseases and support the multi-pathway combination approach of COYA 302 to target numerous components of the dysfunctional immune system. About COYA 302 COYA 302 is an investigational and proprietary biologic combination therapy with a dual immunomodulatory mechanism of action intended to enhance the anti-inflammatory function of regulatory T cells (Tregs) and suppress the inflammation produced by activated monocytes and macrophages. COYA 302 is comprised of proprietary low dose interleukin-2 (LD IL-2) and CTLA-4 Ig and is being developed for subcutaneous administration for the treatment of patients with ALS, FTD, and PD. These mechanisms may have additive or synergistic effects. In February of 2023, Coya announced results from a proof-of-concept, open-label clinical study evaluating commercially available LD IL-2 and CTLA-4 Ig in a small cohort of patients with ALS conducted at the Houston Methodist Research Institute (Houston, Texas) by Stanley Appel, M.D., Jason Thonhoff, M.D., Ph.D., and David Beers, Ph.D. This study was the first-of-its-kind evaluating this dual-mechanism immunotherapy for the treatment of ALS. Patients in the study received investigational treatment for 48 consecutive weeks and were evaluated for safety and tolerability, Treg function, serum biomarkers of oxidative stress and inflammation, and clinical functioning as measured by the ALSFRS-R scale. During the 48-week treatment period, the therapy was well tolerated. The most common adverse event was mild injection-site reactions. No patient discontinued the study, and no deaths or other serious adverse events were reported. Patients' disease progression was measured using the ALSFRS-R scale, a validated rating tool for monitoring the progression of disability in patients with ALS. The mean (±SD) ALSFRS-R scores at week 24 (33.75 ±3.3) and week 48 (32 ±7.8) after initiation of treatment were not statistically different compared to the ALSFRS-R score at baseline (33.5 ±5.9), suggesting significant amelioration in the progression of the disease over the 48-week treatment period. Treg suppressive function, expressed as percentage of inhibition of proinflammatory T cell proliferation, showed a statistically significant increase over the course of the treatment period and was significantly reduced at the end of the 8-week washout post-treatment period. Treg suppressive function at 24 weeks (79.9 ±9.6) and 48 weeks (89.5 ±4.1) were significantly higher compared to baseline (62.1 ±8.1) (p<0.01), suggesting enhanced and durable Treg suppressive function over the course of treatment. In contrast, Treg suppressive function (mean ±SD) was significantly decreased at the end of the 8-week washout period compared to end-of-treatment at week 48 (70.3 ±8.1 vs. 89.5 ±4.1, p <0.05). The study also evaluated serum biomarkers of inflammation, oxidative stress, and lipid peroxides. The available data up to 16 weeks after initiation of treatment suggest a decrease in these biomarker levels, which is consistent with the observed enhancement of Treg function. The evaluation of the full biomarker data is ongoing. COYA 302 is an investigational product not yet approved by the FDA or any other regulatory agency. About Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's Disease, is a rare neurological disease that affects motor neurons, the nerve cells in the brain and spinal cord that control voluntary muscle movement. About 20,000 people live with ALS in the United States and approximately 5,000 new cases are diagnosed every year. The disease is progressive, meaning the symptoms get worse over time. The functional status of ALS patients declines about 1 point per month on average, as measured by the Revised ALS Function Rating Scale1, or ALSFRS-R, a validated tool to monitor the progression of the disease. ALS has no cure, and the currently approved drug treatments provide limited benefit to patients. ALS is a type of motor neuron disease. As motor neurons degenerate and die, they stop sending messages to the muscles, which causes the muscles to weaken, start to twitch (fasciculations), and waste away (atrophy). Eventually, the brain loses its ability to initiate and control voluntary movements. Most people with ALS die from respiratory failure, usually within three to five years from when the symptoms first appear.2 About Frontotemporal Dementia Frontotemporal dementia (FTD) is the result of damage to neurons in the frontal and temporal lobes of the brain. Many possible symptoms can result, including unusual behaviors, emotional problems, trouble communicating, difficulty with work, or difficulty with walking. FTD is rare and tends to occur at a younger age than other forms of dementia. About 60% of people with FTD are 45 to 64 years old. FTD is progressive, meaning symptoms get worse over time. In the early stages, people may have just one symptom. As the disease progresses, other symptoms appear as more parts of the brain are affected. It is difficult to predict how long someone with FTD will live. Some people live more than 10 years after diagnosis, while others live less than two years after they are diagnosed. There is no cure for FTD, and no treatments slow or stop the progression of the disease.3 References Atassi N, et al. The PRO-ACT database: design, initial analyses, and predictive features. Neurology, 2014;83:1719–1725. doi: 10.1212/WNL.0000000000000951. National Institutes of Health (NIH) Website ( ), accessed on January 8, 2024. National Institutes of Health (NIH) Website ( ), accessed on January 8, 2024. About Coya Therapeutics, Inc. Headquartered in Houston, TX, Coya Therapeutics, Inc. (Nasdaq: COYA) is a clinical-stage biotechnology company developing proprietary treatments focused on the biology and potential therapeutic advantages of regulatory T cells (“Tregs”) to target systemic inflammation and neuroinflammation. Dysfunctional Tregs underlie numerous conditions, including neurodegenerative, metabolic, and autoimmune diseases, and this cellular dysfunction may lead to sustained inflammation and oxidative stress resulting in lack of homeostasis of the immune system. Coya’s investigational product candidate pipeline leverages multiple therapeutic modalities aimed at restoring the anti-inflammatory and immunomodulatory functions of Tregs. Coya’s therapeutic platforms include Treg-enhancing biologics, Treg-derived exosomes, and autologous Treg cell therapy. COYA 302 – the Company’s lead biologic investigational product or “Pipeline in a Product”– is a proprietary combination of COYA 301 (Coya’s proprietary LD IL-2) and CTLA4-Ig for subcutaneous administration with a unique dual mechanism of action that is now being developed for the treatment of Amyotrophic Lateral Sclerosis, Frontotemporal Dementia, Parkinson’s Disease, and Alzheimer’s Disease. Its multi-targeted approach enhances the number and anti-inflammatory function of Tregs and simultaneously lowers the expression of activated microglia and the secretion of pro-inflammatory mediators. This synergistic mechanism may lead to the re-establishment of immune balance and amelioration of inflammation in a sustained and durable manner that may not be achieved by either low-dose IL-2 or CTLA4-Ig alone. For more information about Coya, please visit Forward-Looking Statements This press release contains “forward-looking” statements that are based on our management’s beliefs and assumptions and on information currently available to management. Forward-looking statements include all statements other than statements of historical fact contained in this presentation, including information concerning our current and future financial performance, business plans and objectives, current and future clinical and preclinical development activities, timing and success of our ongoing and planned clinical trials and related data, the timing of announcements, updates and results of our clinical trials and related data, our ability to obtain and maintain regulatory approval, the potential therapeutic benefits and economic value of our product candidates, competitive position, industry environment and potential market opportunities. The words “believe,” “may,” “will,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” and similar expressions are intended to identify forward-looking statements. Forward-looking statements are subject to known and unknown risks, uncertainties, assumptions and other factors including, but not limited to, those related to risks associated with the impact of COVID-19; the success, cost and timing of our product candidate development activities and ongoing and planned clinical trials; our plans to develop and commercialize targeted therapeutics; the progress of patient enrollment and dosing in our preclinical or clinical trials; the ability of our product candidates to achieve applicable endpoints in the clinical trials; the safety pro our product candidates; the potential for data from our clinical trials to support a marketing application, as well as the timing of these events; our ability to obtain funding for our operations; development and commercialization of our product candidates; the timing of and our ability to obtain and maintain regulatory approvals; the rate and degree of market acceptance and clinical utility of our product candidates; the size and growth potential of the markets for our product candidates, and our ability to serve those markets; our commercialization, marketing and manufacturing capabilities and strategy; future agreements with third parties in connection with the commercialization of our product candidates; our expectations regarding our ability to obtain and maintain intellectual property protection; our dependence on third party manufacturers; the success of competing therapies or products that are or may become available; our ability to attract and retain key scientific or management personnel; our ability to identify additional product candidates with significant commercial potential consistent with our commercial objectives; and our estimates regarding expenses, future revenue, capital requirements and needs for additional financing. We have based these forward-looking statements largely on our current expectations and projections about future events and trends that we believe may affect our financial condition, results of operations, business strategy, short-term and long-term business operations and objectives, and financial needs. Moreover, we operate in a very competitive and rapidly changing environment, and new risks may emerge from time to time. It is not possible for our management to predict all risks, nor can we assess the impact of all factors on our business or the extent to which any factor, or combination of factors, may cause actual results to differ materially from those contained in any forward-looking statements we may make. In light of these risks, uncertainties and assumptions, the forward-looking events and circumstances discussed herein may not occur and actual results could differ materially and adversely from those anticipated or implied in the forward-looking statements. Although our management believes that the expectations reflected in our forward-looking statements are reasonable, we cannot guarantee that the future results, levels of activity, performance or events and circumstances described in the forward-looking statements will be achieved or occur. We undertake no obligation to publicly update any forward-looking statements, whether written or oral, that may be made from time to time, whether as a result of new information, future developments or otherwise.

Cleared First Four Monotherapy Doses and Initial Combination Cohort with No Dose Limiting Toxicities at any Dose Level KVA12123 Monotherapy Demonstrated Dose Proportional Induction of Pro-inflammatory Biomarkers Required for Strong Anti-tumor Activity Additional Monotherapy Clinical Efficacy Data and Initial Combination Clinical Data Anticipated in Q2 2024 Jan. 17, 2024 -- Kineta, Inc. (Nasdaq: KA), a clinical-stage biotechnology company focused on the development of novel immunotherapies in oncology that address cancer immune resistance, announced today an update on its ongoing VISTA-101 Phase 1/2 clinical trial evaluating KVA12123 in patients with advanced solid tumors. KVA12123, Kineta’s novel VISTA blocking immunotherapy, cleared the first four monotherapy dose levels and the first cohort in combination with Merck’s anti-PD-1 therapy, KEYTRUDA® (pembrolizumab). KVA12123 was well tolerated with no dose limiting toxicities (DLT) or cytokine related adverse events at any dose level. Additionally, KVA12123 demonstrates robust and dose proportional induction of pro-inflammatory biomarkers required for strong anti-tumor activity, demonstrating on target effects of blocking VISTA. “We are encouraged with the efficacy-related biomarker data that demonstrate on-target activity of KVA12123 in our Phase 1/2 clinical trial. Additionally, the safety profile supports advancing to higher doses in the monotherapy and combination cohorts of the study,” said Shawn Iadonato, Ph.D., Chief Executive Officer of Kineta. “We believe KVA12123 continues to show its potential as a next-generation immunotherapy that may overcome immunosuppression in the tumor microenvironment. The clinical study is progressing on time, and we anticipate fully enrolling the Phase 1 portion of the trial by April 2024.” In the VISTA-101 trial (NCT05708950), a total of 18 patients have been dosed with KVA12123. 15 patients with advanced solid tumors were enrolled in the first four monotherapy dose-escalation cohorts, where subjects received either 3, 10, 30 or 100 mg of KVA12123 by intravenous (IV) infusion every two weeks. Additionally, 3 patients were enrolled in the initial combination cohort with 30 mg KVA12123 and 400mg of pembrolizumab. Primary objectives of the Phase 1/2 study are to evaluate the safety and tolerability of KVA12123 and to determine the recommended Phase 2 dose (RP2D). Patients enrolled in the study were heavily pretreated with multiple prior lines of therapy including chemotherapy, radiation, and immunotherapy. Approximately half of the enrolled patients failed prior checkpoint inhibitor therapy. Dosing of the 300 mg monotherapy and 100 mg in combination with pembrolizumab cohorts have been initiated. In the first four monotherapy cohorts and initial cohort in combination with pembrolizumab, KVA12123 was well tolerated at all doses and no DLTs were observed. During Phase 1, the study is closely monitoring the proinflammatory IL-6 and TNFα cytokines that are associated with cytokine release syndrome (CRS). No evidence of CRS-associated cytokine induction has been observed at any dose level with KVA12123 in the initial cohorts. KVA12123 demonstrated dose proportional induction of pro-inflammatory biomarkers including CXCL10, CCL2, CCL3 and CCL4 that are required for strong anti-tumor activity. Consistent increases in anti-tumor non-classical monocytes, NK cells, helper (CD4+) and cytotoxic (CD8+) T cells in the blood were also observed. These key pro-inflammatory myeloid derived cytokines and chemokines are involved in immune cell activation and recruitment in the tumor microenvironment (TME). To guide the recommended Phase 2 dose (RP2D) decision, Kineta developed a proprietary assay to evaluate VISTA RO on immune cells from patients in the clinical trial. KVA12123 achieved a greater than 90% VISTA RO at the 30 and 100 mg doses. Furthermore, pharmacokinetic analyses demonstrated a greater than dose-proportional increase in drug exposure across all evaluated doses, consistent with target-mediated drug disposition at lower doses. “We are pleased to see the compelling safety data of KVA12123 and lack of CRS-associated cytokine induction. The drug has been very well tolerated in patients,” said Thierry Guillaudeux, Ph.D., Chief Scientific Officer of Kineta. “These data are encouraging and consistent with the results from our preclinical models.” Kineta (Nasdaq: KA) is a clinical-stage biotechnology company with a mission to develop next-generation immunotherapies that transform patients’ lives. Kineta has leveraged its expertise in innate immunity and is focused on discovering and developing potentially differentiated immunotherapies that address the major challenges with current cancer therapy. The company’s immuno-oncology pipeline includes KVA12123, a novel VISTA blocking immunotherapy currently in a Phase 1/2 clinical trial in patients with advanced solid tumors, and a preclinical monoclonal antibody targeting CD27. For more information on Kineta, please visit www.kinetabio.com, and follow Kineta on Twitter, LinkedIn and Facebook. KVA12123 is a VISTA blocking immunotherapy in development as a twice weekly monoclonal antibody infusion drug being evaluated in a Phase 1/2 clinical trial for patients with advanced solid tumors. Competitive therapies targeting VISTA have demonstrated either poor monotherapy anti-tumor activity in preclinical models or induction of cytokine release syndrome (CRS) in human clinical trials. Through the combination of unique epitope binding and an optimized IgG1 Fc region, KVA12123 demonstrates strong monotherapy tumor growth inhibition in preclinical models without evidence of CRS in clinical trial participants. KVA12123 has been shown to de-risk the VISTA target and provides a novel approach to address immune suppression in the TME with a mechanism of action that is differentiated and complementary with T cell focused therapies. KVA12123 may be an effective immunotherapy for many types of cancer including non-small cell lung (NSCLC), colorectal, renal cell carcinoma, head and neck, and ovarian cancer. VISTA (V-domain Ig suppressor of T cell activation) is a negative immune checkpoint that suppresses T cell function in a variety of solid tumors. High VISTA expression in tumor correlates with poor survival in cancer patients and has been associated with a lack of response to other immune checkpoint inhibitors. Blocking VISTA induces an efficient polyfunctional immune response to address immunosuppression and drives anti-tumor responses. The content above comes from the network. if any infringement, please contact us to modify.

Head-to-head study between eblasakimab and dupilumab in skin biopsies from atopic dermatitis (AD) patients confirm eblasakimab’s differentiated effects of targeting IL-13R vs IL-4RUsing an established COPD model of human lung slices, new data demonstrate eblasakimab’s potential to reduce airway constriction and enhance dilationResults demonstrate for the first time the potential utility of eblasakimab in other indications beyond AD SAN MATEO, Calif. and SINGAPORE, Nov. 03, 2023 (GLOBE NEWSWIRE) -- ASLAN Pharmaceuticals (Nasdaq: ASLN), a clinical-stage, immunology-focused biopharmaceutical company developing innovative treatments to transform the lives of patients, today announced new data was presented at the Dermatology Drug Development Summit (DDDS) that took place in Boston, MA, from October 31 to November 2, 2023. The datasets presented strengthen evidence for eblasakimab’s differentiated mechanism of action in atopic dermatitis (AD), and, for the first time, show application in a new indication, chronic obstructive pulmonary disease (COPD), which can be driven by Type 2 inflammation. A head-to-head study between eblasakimab and dupilumab conducted in skin punch biopsies of AD patients showed differential expression of inflammatory cytokines secreted by the localized skin tissue, with eblasakimab treatment more efficiently reducing expression of Th2 cytokines IL-13, IL-4 and sCD40L, as well as IL-17F and chemokines CCL3 and CCL4, compared to dupilumab treatment. These preliminary results validate previously published data1 from AD patient peripheral blood mononuclear cells from ASLAN’s research collaboration with Dr Shawn Kwatra (Johns Hopkins Medicine) and Dr Madan Kwatra (Duke University). These data together demonstrate eblasakimab’s differentiated effects compared to dupilumab and highlight the potential advantages to targeting IL-13R with eblasakimab, which may lead to more efficient blockade of Type 2 signaling while also sparing the Type 1 receptor. ASLAN also presented new data investigating the role of eblasakimab in COPD using an established ex vivo model of precision cut lung slices from human donors2. The model tested airway hyperresponsiveness (AHR) in the lung tissue using IL-4 and IL-13, the key Th2 cytokines involved in COPD disease pathology3. Eblasakimab significantly reduced IL-4 and IL-13-induced AHR by reducing airway constriction. Furthermore, IL-4 and IL-13 sensitized the airways to further constriction in response to methacholine, but this sensitization was blocked by eblasakimab treatment. To examine the effects on airway dilation, formoterol was used to induce bronchodilation. IL-4 and IL-13 pre-treatment significantly decreased dilation in response to formoterol within 5 minutes of treatment, but these effects were effectively reversed by eblasakimab, restoring the airway’s normal response. Hence, eblasakimab successfully blocked IL-4/IL-13 induced AHR in lung tissue and restored the normal response of airway constriction and dilation which are of clinical significance in COPD. Eblasakimab blocks both IL-4 and IL-13 through the Type 2 receptor, giving it the potential to be more effective in a broader range of indications compared to drugs that only target the IL-13 cytokine. “COPD is the third most common cause of mortality globally4 and is a heterogeneous disease with a significant proportion of patients affected by Type 2-driven pathology that have a limited range of targeted treatment options. The data we have presented in the translational models are key to exploring the potential of eblasakimab in other indications beyond AD, and we believe that there is great potential for eblasakimab to provide an effective and differentiated treatment option for COPD, a market that is expected to be $30 billion by 20325,” said Dr Carl Firth, Chief Executive Officer at ASLAN Pharmaceuticals. “While eblasakimab has already demonstrated a monthly dosing regimen in AD without compromising on efficacy, there is a vast unexplored potential in other diseases driven by the common underlying biology of Type 2 inflammation.” “The translational data we have presented provide evidence of eblasakimab’s unique mechanism of action and highlight its differentiation from drugs targeting the IL-4R,” said Dr Ferda Cevikbas, Head, Translational Science at ASLAN Pharmaceuticals. “We are grateful for the invitation to present these translational models at this industry conference and showcase eblasakimab’s potential to address Type 2-driven inflammation across AD and COPD.” Studies in both translational models are ongoing and ALSAN plans to submit comprehensive data sets for publication to upcoming scientific meetings. The presentation from Drug Development Summit can be accessed via the ASLAN website here. Cevikbas et al (2023) 1st International Society of Investigative Dermatology Meeting, in late-breaker minisymposiumKim et al (2023) Science Advances 9 (20)Miotto et al (2003) Eur Resp J 22:602-608World Health Organization (2023). Chronic obstructive pulmonary disease (COPD). Accessed 2 November 2023Precedence Research (2023) COPD Treatment Market About eblasakimab Eblasakimab is a potential first-in-class monoclonal antibody targeting the IL-13 receptor subunit of the Type 2 receptor, a key pathway driving several allergic inflammatory diseases. Eblasakimab’s unique mechanism of action enables specific blockade of the Type 2 receptor and has the potential to improve upon current biologics used to treat allergic disease. By blocking the Type 2 receptor, eblasakimab prevents signaling through both interleukin 4 (IL-4) and interleukin 13 (IL-13) – the key drivers of inflammation in AD. Positive results from the Phase 2b TREK-AD study in moderate-to-severe AD support eblasakimab’s potential to deliver a monthly dosing regimen from initiation in AD without compromising on efficacy and with an encouraging safety profile demonstrated to date, with preparations for Phase 3 underway. ASLAN is also investigating eblasakimab in dupilumab experienced, moderate-to-severe AD patients in the Phase 2 trial, TREK-DX. About ASLAN Pharmaceuticals ASLAN Pharmaceuticals (Nasdaq: ASLN) is a clinical-stage, immunology-focused biopharmaceutical company developing innovative treatments to transform the lives of patients. ASLAN is developing eblasakimab, a potential first-in-class antibody targeting the IL-13 receptor in moderate-to-severe atopic dermatitis (AD) with the potential to improve upon current biologics used to treat allergic disease, and has recently reported positive topline data from a Phase 2b dose ranging study in moderate-to-severe AD. ASLAN is also developing farudodstat, a potent oral inhibitor of the enzyme dihydroorotate dehydrogenase (DHODH) as a potential first-in-class treatment for alopecia areata (AA) in a Phase 2a proof-of-concept trial with an interim readout expected in 1Q 2024. ASLAN has teams in San Mateo, California, and in Singapore. For additional information please visit the website or follow ASLAN on LinkedIn. Forward-looking statements This release contains forward-looking statements. These statements are based on the current beliefs and expectations of the management of ASLAN Pharmaceuticals Limited and/or its affiliates (the “Company”). These forward-looking statements may include, but are not limited to statements regarding the Company’s business strategy and clinical development plans; the Company’s plans to develop and commercialize eblasakimab and farudodstat; the safety and efficacy of eblasakimab and farudodstat; the Company’s plans and expected timing with respect to manufacturing activities, clinical trials, clinical trial enrolment and clinical trial results for eblasakimab and farudodstat; the potential of eblasakimab as a first-in-class treatment for atopic dermatitis and of farudodstat as a first-in-class treatment for alopecia areata; the potential benefits, capabilities and results of the Company’s collaboration efforts; and the Company’s cash runway. The Company’s estimates, projections and other forward-looking statements are based on management's current assumptions and expectations of future events and trends, which affect or may affect the Company’s business, strategy, operations, or financial performance, and inherently involve significant known and unknown risks and uncertainties. Actual results and the timing of events could differ materially from those anticipated in such forward-looking statements as a result of many risks and uncertainties, which include, unexpected safety or efficacy data observed during preclinical or clinical studies; the fact that results of earlier studies and trials may not be predictive of future trial results; clinical site activation rates or clinical trial enrolment rates that are lower than expected; the impact of the COVID-19 pandemic, the ongoing conflict between Ukraine and Russia and bank failures on the Company’s business and the global economy; general market conditions; changes in the competitive landscape; and the Company’s ability to obtain sufficient financing to fund its strategic and clinical development plans. Other factors that may cause actual results to differ from those expressed or implied in such forward-looking statements are described in the Company’s US Securities and Exchange Commission filings and reports (Commission File No. 001- 38475), including the Company’s Annual Report on Form 20-F filed with the US Securities and Exchange Commission on March 24, 2023. All statements other than statements of historical fact are forward-looking statements. The words “believe,” “may,” “might,” “could,” “will,” “aim,” “estimate,” “continue,” “anticipate,” “intend,” “expect,” “plan,” or the negative of those terms, and similar expressions that convey uncertainty of future events or outcomes are intended to identify estimates, projections, and other forward-looking statements. Estimates, projections, and other forward-looking statements speak only as of the date they were made, and, except to the extent required by law, the Company undertakes no obligation to update or review any estimate, projection, or forward-looking statement. ASLAN Media and IR contacts Emma ThompsonAshley R. RobinsonSpurwing CommunicationsLifeSci Advisors, LLCTel: +65 6206 7350Tel: +1 (617) 430-7577Email: ASLAN@spurwingcomms.comEmail: arr@lifesciadvisors.com