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WTX-518, a conditionally activated IL-18 INDUKINETM molecule that resists suppression by IL-18BP, led to complete tumor regressions in preclinical models WTX-712, a conditionally activated IL-21 INDUKINETM molecule has potent antitumor activity in preclinical models with a differentiated immune activation mechanism WATERTOWN, Mass., April 05, 2024 (GLOBE NEWSWIRE) -- Werewolf Therapeutics Inc. (the “Company” or “Werewolf”) (Nasdaq: HOWL), an innovative biopharmaceutical company pioneering the development of conditionally-activated therapeutics engineered to stimulate the body’s immune system for the treatment of cancer, is presenting preclinical data on development candidates WTX-518 and WTX-712 in posters at the American Association for Cancer Research (AACR) Annual Meeting, taking place April 5-10 in San Diego, California. “We are excited to share that both WTX-518 and WTX-712 demonstrate powerful immunotherapeutic effects in preclinical models,” said Daniel J. Hicklin, Ph.D., President and Chief Executive Officer of Werewolf. “WTX-518 exhibits remarkable tumor-selective activation, resistance to IL-18BP and robust immune activation, overcoming key hurdles in the use of this promising cytokine in cancer therapy. WTX-712 acts through a unique mechanism that robustly activates tumor-specific T lymphocytes with an expanded therapeutic window through its selective release of wild-type IL-21 in the TME. These data collectively highlight the innovative strategies we are pursuing to further expand the repertoire of unique immune stimulating cytokine mechanisms in the fight against cancer.” Results highlighting WTX-518 findings are summarized in a poster titled, “Discovery of WTX-518, an IL-18 pro-drug that is conditionally activated within the tumor microenvironment and induces regressions in mouse tumor models” (Abstract #4074). Key takeaways reveal that WTX-518: is inducible, and its in vitro activity is not impeded by IL-18BP; selectively delivers active binding protein resistant (BPR) IL-18 to the tumor microenvironment (TME); and promotes increased influx and activation of NK cells and polyfunctional CD8 T cells in the TME, and demonstrates complete tumor regression in the MC38 mouse tumor model. The WTX-712 data are summarized in a poster titled, “WTX-712, a conditionally active IL-21 INDUKINE™ molecule, induces a strong anti-tumor phenotype through a differentiated mechanism” (Abstract #4078). Key takeaways reveal that: WTX-712 demonstrates inducibility and antitumor activity with regressions in the MC38 mouse tumor model; IL-21 HLE (half-life extended) has superior anti-tumor efficacy compared to IL-2 HLE therapy in mouse tumor models that are highly resistant to anti-PD-1/PD-L1 treatment, in part due to the activation of type-I IFN pathways; and IL-21 HLE promotes sustained expansion and activation of tumor infiltrating CD8 T cells with increased polyfunctionality and induces expression of cytotoxic effector molecules (Granzyme A, Granzyme B, and perforin). Both posters can be viewed in person from 9:00 a.m. to 12:30 p.m. PDT on Tuesday, April 9, during the session category “Immunology” at Poster Section 4, and will be available on our website at Werewolf plans to develop WTX-518 and WTX-712 as potential immunotherapies in refractory and/or immunologically unresponsive tumors. About Werewolf Therapeutics Werewolf Therapeutics, Inc., is an innovative biopharmaceutical company pioneering the development of therapeutics engineered to stimulate the body’s immune system for the treatment of cancer. We are leveraging our proprietary PREDATOR™ platform to design conditionally activated molecules that stimulate both adaptive and innate immunity with the goal of addressing the limitations of conventional proinflammatory immune therapies. Our INDUKINE™ molecules are intended to remain inactive in peripheral tissue yet activate selectively in the tumor microenvironment. Our most advanced clinical stage product candidates, WTX-124 and WTX-330, are systemically delivered, conditionally activated Interleukin-2 (IL-2), and Interleukin-12 (IL-12) INDUKINE molecules, respectively, for the treatment of solid tumors. We expect to advance WTX-124 in multiple tumor types as a single agent and in combination with an immune checkpoint inhibitor and WTX-330 in multiple tumor types or Non-Hodgkin Lymphoma as a single agent. To learn more visit . Cautionary Note Regarding Forward-Looking Statements This press release contains forward-looking statements that involve substantial risk and uncertainties. All statements, other than statements of historical facts, contained in this press release, including statements regarding Werewolf’s future operations, prospects, plans, and the potential activity and efficacy of product candidates in preclinical studies constitute forward-looking statements within the meaning of The Private Securities Litigation Reform Act of 1995. The words “aim,” “anticipate,” “believe,” “contemplate,” “continue,” “could,” “design,” “designed to,” “estimate,” “expect,” “goal,” “intend,” “may,” “might,” “objective,” “ongoing,” “plan,” “potential,” “predict,” “project,” “promise,” “should,” “target,” “will,” or “would,” or the negative of these terms, or other comparable terminology are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. The Company may not actually achieve the plans, intentions or expectations disclosed in these forward-looking statements, and you should not place undue reliance on these forward-looking statements. Actual results or events could differ materially from the plans, intentions and expectations disclosed in these forward-looking statements as a result of various important factors, including: uncertainties inherent in the development of product candidates, including the conduct of research activities, the initiation and completion of preclinical studies and clinical trials; uncertainties as to the availability and timing of results from preclinical studies; the timing of and the Company’s ability to submit and obtain regulatory approval for investigational new drug applications; whether results from preclinical studies will be predictive of the results of later preclinical studies and clinical trials; the Company’s ability to obtain sufficient cash resources to fund the Company’s foreseeable and unforeseeable operating expenses and capital expenditure requirements; the impact of the COVID-19 pandemic on the Company’s business and operations; as well as the risks and uncertainties identified in the “Risk Factors” section of the Company’s most recent Form 10-K filed with the Securities and Exchange Commission (“SEC”), and in subsequent filings the Company may make with the SEC. In addition, the forward-looking statements included in this press release represent the Company’s views as of the date of this presentation. The Company anticipates that subsequent events and developments will cause its views to change. However, while the Company may elect to update these forward-looking statements at some point in the future, it specifically disclaims any obligation to do so. These forward-looking statements should not be relied upon as representing the Company’s views as of any date subsequent to the date of this press release. Investor Contact: Josh Rappaport Stern IR 212.362.1200 Josh.Rappaport@sternir.com Media Contact: Amanda Sellers VERGE Scientific Communications 301.332.5574 asellers@vergescientific.com Company Contact: Ellen Lubman Chief Business Officer Werewolf Therapeutics elubman@werewolftx.com

68% of patients treated with ELI-002 developed cytotoxic mKRAS-specific CD4+ T cells 84% of patients treated with ELI-002 developed cytotoxic mKRAS-specific CD8+ T cells The majority of ELI-002-treated patients tested had antigen spreading where induced T cells targeted additional patient-specific tumor mutations beyond mKRAS The majority of patients who received a ELI-002 booster dose were observed to have durable mKRAS-specific T cell response with increased memory T cell phenotype Preclinical studies of ELI-007 and ELI-008 demonstrated that AMP vaccination resulted in a 42-fold to a several-hundred-fold increased immune response when compared to conventional vaccines Initial ELI-002 7P clinical data expected to be presented in the second quarter of 2024 BOSTON, April 05, 2024 (GLOBE NEWSWIRE) -- Elicio Therapeutics, Inc. (Nasdaq: ELTX, “Elicio Therapeutics” or “Elicio”), a clinical-stage biotechnology company developing a pipeline of novel immunotherapies for the treatment of cancer, today announced that it will be sharing pipeline updates for all investigational candidates at the upcoming American Association for Cancer Research (“AACR”) Annual Meeting, taking place in San Diego, California from April 5-10, 2024. Among the data presented will be updated immunogenicity data from the ongoing Phase 1 (AMPLIFY-201) study of ELI-002, an off-the-shelf investigational therapeutic cancer vaccine for patients with mutant Kirsten rat sarcoma (“mKRAS”)-driven pancreatic and colorectal cancers. Preclinical data on vaccine candidates, ELI-007 and ELI-008, investigational peptide vaccines targeting BRAF and p53-driven cancers, respectively, will also be shared. In the first-in-human, Phase 1 (AMPLIFY-201) study, ELI-002 was given as adjuvant treatment for patients with high relapse-risk mKRAS-driven colorectal cancer (“CRC”) and pancreatic ductal adenocarcinoma (“PDAC”). A majority of patients who received the booster immunizations maintained or increased mKRAS-specific T cell responses relative to baseline. ELI-002 demonstrated several key advantages, including lymph node-targeted vaccine design, potent immunogenicity with balanced CD4+ and CD8+ T cell responses, HLA-agnostic activity, and targeting of mKRAS antigens critical for tumor survival. The mKRAS-specific CD4 and CD8 T cells generated by ELI-002 exhibited increased cytotoxic function and development of favorable memory phenotype. Regulatory T cell responses were not detected. Antigen spreading was observed following ELI-002 vaccination, with patient-specific tumor neoantigen-directed T cell responses detected in the majority of evaluated patients using direct ex vivo immunogenicity assays. "Earlier data published in Nature Medicine demonstrate that our off-the-shelf lymph node-targeted cancer vaccine candidate, ELI-002, induces memory T cell responses. With longer follow-up, we observed response durability and added antigen-spreading to the mechanism of ELI-002, where we saw additional personal neoantigen responses join together with mutated KRAS responses creating a precision response that may lead to enhanced clinical activity,” said Christopher Haqq, M.D., Ph.D., Elicio’s Executive Vice President, Head of Research and Development, and Chief Medical Officer. “Following positive early findings from the 2-peptide formulation of ELI-002, we initiated a randomized Phase 2 study of our 7-peptide formulation, ELI-002 7P, in adjuvant pancreatic cancer (NCT05726864). We expect to share interim 7-peptide ELI-002 data from the Phase 1A arm in the second quarter of 2024.” Peter DeMuth, Ph.D., Chief Scientific Officer at Elicio Therapeutics, added, “These preclinical data demonstrate that ELI-007 and ELI-008 induce strong tumor antigen-specific T cell responses targeting BRAF and p53 mutations, respectively. ELI-007 and ELI-008 induced highly potent and functional T cell responses, often ten to a hundred-fold higher than comparator. These data build on previous data showing that the AMP strategy can improve the potency of vaccine immunotherapy by delivering vaccine components directly to the lymph nodes, the ‘command center’ of the immune system. These data support the broad applicability of the technology and represent promising therapeutic product opportunities targeting mutations shared in a large fraction of human solid cancers.” Poster Presentation Summary Presentation Title: Durable immunogenicity of ELI-002 2P in AMPLIFY-201: Lymph node targeted mKRAS-specific amphiphile vaccine in pancreatic and colorectal cancer Session Title: First-in-Human Phase I Clinical Trials 1 Session Date and Time: Monday, April 8, 2024, 1:30 PM – 5:00 PM PT ELI-002 2P consists of 2 Amph-modified mKRAS peptide antigens, Amph-G12D and Amph-G12R (Amph-Peptides 2P), and an Amph-modified immune-stimulatory oligonucleotide adjuvant (Amph-CpG-7909). ELI-002 2P was administered as an adjuvant treatment for patients with high relapse-risk mutant KRAS PDAC and CRC. 25 patients received ELI-002 2P at 1.4 mg of Amph-Peptides 2P and Amph-CpG-7909 at 5 escalating dose levels: 0.1, 0.5, 2.5, 5, and 10 mg. Peripheral blood and circulating tumor DNA (“ctDNA”) or serum tumor antigen were collected longitudinally to assess T cell immunogenicity and reductions in clinical tumor biomarkers. A majority of patients who received ELI-002 booster immunizations maintained or increased mKRAS-specific T cell responses relative to baseline. Durable responses were associated with increased memory T cell phenotype compared to baseline. ELI-002 induced increased mKRAS-specific CD4 and CD8 T cells with cytotoxic function, associated with increased memory phenotype in a majority of patients. CD4+ T regulatory cells were not induced after ELI-002 2P immunization. Antigen spreading was observed with T cell responses to patient-specific tumor mutations (not mKRAS) after ELI-002 2P vaccination in a majority of patients tested. Data demonstrated several advantages of ELI-002 including lymph node-targeted vaccine design, potent immunogenicity with durable and balanced CD4+ and CD8+ T cell responses, increased T cell cytotoxic function, and antigen spreading to induce T cells targeting additional tumor mutations beyond mKRAS. Presentation Title:AMP-peptide vaccination against mutant BRAF epitopes promotes lymph node delivery to generate potent, functional T cell immunity Session Title: Vaccines, Antigens, and Antigen Presentation 1 Session Date and Time: Tuesday, April 9, 2024, 9:00 AM – 12:30 PM PT Our preclinical program, ELI-007, is an investigational multivalent lymph node–targeted AMP peptide vaccine comprised of the V600E and V600K mutant antigens, developed to target BRAF gene mutations. AMP-immunization generated robust in vivo immune responses yielding strong T cell activation against mBRAF epitopes. Lymph node-targeted AMP-vaccination resulted in a 19-fold increase in immune response after only 3 doses and a 42-fold increase after 5 doses when compared to conventional comparator vaccines. Induced T cells were polyfunctional exhibiting the production of multiple effector cytokines (IFNγ, TNFα, IL2, GM-CSF) as well as cytotoxic molecules (Granzyme B) important in the lysis of tumor cells. Substantial populations of mBRAF-specific T cells were found patrolling peripheral organs like the lung, which is one of the predominant sites for metastatic spread in melanoma and colorectal carcinoma. Presentation Title: AMP-peptide vaccination against multiple p53 mutant epitopes promotes lymph node delivery to generate potent, functional T cell immunity Session Title: Vaccines, Antigens, and Antigen Presentation 1 Session Date and Time: Tuesday, April 9, 2024, 9:00 AM – 12:30 PM PT Our preclinical program, ELI-008, is an investigational multivalent lymph node–targeted AMP peptide vaccine developed to target p53 hotspot mutations. AMP-immunization generated robust immune responses yielding strong T cell activation against common p53 hot spot mutations (R248W, R248Q, R175H, R273H, R273C, R282W, G245S, Y220C, C135Y, R158H, H214R). Potent T cell responses were observed after only two doses with AMP-p53 R248W, which were further improved after a third bi-weekly dose. For multiple p53 mutations, ELI-008 demonstrated a several-hundred-fold increase over conventional comparator vaccines. Induced T cells were polyfunctional exhibiting production of multiple effector cytokines (IFNγ, TNFα, IL2, GM-CSF) and showed high cytotoxic potential by secreting large quantities of Granzyme B and effectively killing target cells in vivo. Substantial populations of p53-specific T cells were found patrolling peripheral organs like the lung, which is one of the predominant sites for the metastatic spread of many cancers. About ELI-002 Our lead product candidate, ELI-002, is a structurally novel investigational AMP cancer vaccine that targets cancers that are driven by mutations in the mKRAS-gene—a prevalent driver of many human cancers. ELI-002 is comprised of two powerful components that are built with our AMP platform consisting of AMP-modified mutant KRAS peptide antigens and an AMP-modified CpG adjuvant that is available as an off-the-shelf subcutaneous administration. ELI-002 2P (2 peptide formulation) is currently being studied in an ongoing Phase 1 (AMPLIFY-201) trial in patients with high relapse risk mKRAS-driven solid tumors, following surgery and chemotherapy (NCT04853017). ELI-002 7P (7 peptide formulation) is currently being studied in a Phase 2 (AMPLIFY-7P) trial in patients with mKRAS-driven pancreatic cancer (NCT05726864). The ELI-002 7P formulation is designed to provide immune response coverage against seven of the most common KRAS mutations present in 25% of all solid tumors, thereby increasing the potential patient population for ELI-002 and potentially reducing the chance of bypass resistance mechanisms. About ELI-007 and ELI-008 Our preclinical programs, ELI-007 and ELI-008, are being evaluated in studies funded by the Gastro-Intestinal (“GI”) Research Foundation with the aim of developing multivalent cancer vaccines targeting several mutations. ELI-007 is an investigational multivalent lymph node–targeted AMP peptide vaccine comprised of the V600E and V600K mutant antigens, which make up >95% of all BRAF-driven cancers in humans, representing up to 1.5 million cancer incidences worldwide each year. The BRAF gene is part of an intracellular signaling pathway that drives cell growth and division. BRAF mutations can lead to uncontrolled cell growth and ultimately cancer. ELI-008 is an investigational multivalent lymph node–targeted AMP peptide vaccine developed to target p53 hotspot mutations. p53 is a tumor-suppressing protein that controls the cell cycle, DNA replication and cell division. Mutations in the p53 protein lead to uncontrolled tumor progression and growth. Similar to KRAS, p53 mutations are present in a broad spectrum of cancer types, accounting for >30% of solid tumors. In preclinical models, ELI-007 and ELI-008 have shown strong T cell activation and demonstrated strong induction of tumor-antigen-specific T cell responses. About Elicio Therapeutics Elicio Therapeutics, Inc. (Nasdaq: ELTX) is a clinical-stage biotechnology company advancing a pipeline of novel lymph node-targeted immunotherapies for the treatment of some of the most aggressive cancers. By combining expertise in immunology and immunotherapy, Elicio is harnessing the natural power of the immune system with Amphiphile (“AMP”) Technology which allows for therapeutic payloads to be delivered directly to the lymph nodes, enhancing the immune system’s cancer-fighting capabilities. By targeting cancer immunotherapies to the core of the immune response, AMP aims to optimize the lymph nodes’ natural ability to educate, activate and amplify cancer-specific T cells, which are essential for recognizing and eliminating tumor cells. Engineered to synchronize immunity in these highly potent sites, AMP is built to enhance the magnitude, potency, quality, and durability of the immune response to drive antitumor activity. The Company’s R&D pipeline includes off-the-shelf therapeutic cancer vaccines ELI-002, (targeting mKRAS-driven cancers) as well as ELI-007 and ELI-008 (targeting BRAF-driven cancers and p53 hotspot mutations, respectively). For more information, please visit . Cautionary Note on Forward-Looking Statements Certain statements contained in this communication regarding matters that are not historical facts, are forward-looking statements within the meaning of Section 21E of the Securities Exchange Act of 1934, as amended, and the Private Securities Litigation Reform Act of 1995 (“PSLRA”). These include statements regarding Elicio’s planned clinical programs, including planned clinical trials, the potential of Elicio’s product candidates, including the potential for the AMP strategy to improve the potency of vaccine immunotherapy, the broad applicability of Elicio’s technology and the potential therapeutic product opportunities; the expected participation and presentation at upcoming conferences, and other statements regarding management’s intentions, plans, beliefs, expectations or forecasts for the future, and, therefore, you are cautioned not to place undue reliance on them. No forward-looking statement can be guaranteed, and actual results may differ materially from those projected. Elicio undertakes no obligation to publicly update any forward-looking statement, whether as a result of new information, future events or otherwise, except to the extent required by law. We use words such as “anticipates,” “believes,” “plans,” “expects,” “projects,” “future,” “intends,” “may,” “will,” “should,” “could,” “estimates,” “predicts,” “potential,” “continue,” “guidance,” and similar expressions to identify these forward-looking statements that are intended to be covered by the safe-harbor provisions of the PSLRA. Such forward-looking statements are based on our expectations and involve risks and uncertainties; consequently, actual results may differ materially from those expressed or implied in the statements due to a number of factors, including, but not limited to, Elicio’s plans to develop and commercialize its product candidates, including ELI-002; the timing of the availability of data from Elicio’s clinical trials, including initial data from the AMPLIFY-7P Phase 1 study of ELI-002 7P expected in the second quarter of 2024; Elicio’s plans to research, develop and commercialize its current and future product candidates; Elicio’s ability to successfully collaborate with existing collaborators or enter into new collaborations, and to fulfill its obligations under any such collaboration agreements; and Elicio’s ability to advance ELI-002 outside of PDAC monotherapy and Elicio’s pipeline programs. New factors emerge from time to time, and it is not possible for us to predict all such factors, nor can we assess the impact of each such factor on the 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. These risks are more fully discussed in the Annual Report on Form 10-K that was filed with the SEC on March 29, 2024, under the heading “Risk Factors”, and any subsequent reports and other documents filed from time to time with the SEC. Forward-looking statements included in this release are based on information available to Elicio as of the date of this release. Elicio does not undertake any obligation to update such forward-looking statements to reflect events or circumstances after the date of this release, except to the extent required by law. Media Contact Kristin Politi LifeSci Communications kpoliti@lifescicomms.com 646-876-4783 Investor Relations Contact Heather DiVecchia Elicio Therapeutics IR@elicio.com 857-209-0153

Updated positive interim data showed notable improvements in estimated median overall survival of 28.8 months after experimental treatment with CAN-2409 versus only 12.5 months in control group in borderline resectable pancreatic ductal adenorcarcinoma (PDAC)At 24 months, survival rate was 71.4% in CAN-2409 treated patients versus only 16.7% in the control group after chemoradiation. At 36 months, estimated survival was 47.6% in the CAN-2409 group versus 16.7% in the control groupNo new safety signals were observed, providing further support that multiple injections of CAN-2409 were generally well tolerated, with no dose-limiting toxicities and no cases of pancreatitisPrevious analysis of resected tumors showed dense aggregates of immune cells, including CD8+, cytotoxic tumor infiltrating lymphocytes, and dendritic cells, in PDAC tissue after CAN-2409 administration, confirming activation of a robust antitumoral immune response NEEDHAM, Mass., April 04, 2024 (GLOBE NEWSWIRE) -- Candel Therapeutics, Inc. (Candel or the Company) (Nasdaq: CADL), a clinical stage biopharmaceutical company focused on developing multimodal biological immunotherapies to help patients fight cancer, today announced updated interim survival data from the ongoing randomized phase 2 clinical trial of CAN-2409 plus valacyclovir (prodrug), together with standard of care (SoC) chemoradiation, followed by resection for borderline resectable pancreatic ductal adenocarcinoma (PDAC). Survival data were updated with eight months of further follow-up since the first analysis presented at the 2023 Society for Immunotherapy (SITC) Annual Meeting. Based on the data presented at SITC, the U.S. Food and Drug Administration (FDA) granted Fast Track Designation to the Company for CAN-2409 in combination with valacyclovir for the treatment of patients with PDAC in December 2023. “Given frequent recurrence and short survival with SoC chemotherapy for non-metastatic PDAC, effective new treatment options are urgently needed,” said Garrett Nichols, MD, MS, Chief Medical Officer of Candel. “We are very encouraged by the improved survival associated with CAN-2409, which has been shown to be durable after prolonged follow-up based on the updated data shown in this randomized clinical trial. CAN-2409 was generally well tolerated without significant additional local or systemic toxicity when added to SoC chemoradiation.” Data Highlights as of a March 29, 2024 Data Cut-off, Include: Prolonged and sustained survival was observed after experimental treatment with CAN-2409 in patients with borderline resectable PDAC (n=13) Estimated median overall survival was 28.8 months in the CAN-2409 group versus only 12.5 months in the control group. At 24 months, a survival rate of 71.4% was observed in CAN-2409 treated patients, after SoC chemoradiation and prior to surgery, versus only 16.7% in the control group. At 36 months, a survival rate of 47.6% was estimated in patients who received CAN-2409, together with SoC chemoradiation prior to surgery, versus only 16.7% in the control group. Importantly, 4 out of 7 patients who received CAN-2409 were still alive at the time of data cut-off, with 2 patients surviving more than 50.0 months from enrollment. Only 1 out of 6 patients, randomized to control SoC chemotherapy, remained alive at data cut-off (alive at 50.6 months). Previous analysis of blood and resected tumors showed consistent and robust activation of the immune response after experimental treatment with CAN-2409 In pancreatic tissue of patients treated with CAN-2409 plus prodrug together with SoC (but not SoC alone), dense aggregates of CD8+ granzyme B positive cytotoxic tumor infiltrating lymphocytes, dendritic cells, and B cells were observed in the tumor microenvironment.Increased levels of soluble granzymes B and H, as well as pro-inflammatory cytokines, including IFN-γ, were observed in peripheral blood after CAN-2409 administration, but not after SoC. CAN-2409 continued to be associated with a favorable safety/tolerability profile Addition of CAN-2409 regimen to SoC was generally well tolerated, with no dose-limiting toxicities, including no cases of pancreatitis “The failure of conventional immunotherapy to improve outcomes in pancreatic cancer is attributed to the highly immunosuppressive tumor microenvironment, which is largely devoid of immune cells,” said Paul Peter Tak, MD, PhD, FMedSci, President and Chief Executive Officer of Candel. “The immunological changes induced by CAN-2409, evident in the pancreatic tissue and the peripheral blood after administration, suggest that CAN-2409 is able to change the balance between the tumor and the patient’s anti-tumor immune response, which can convert progressive cancer into a chronic disease associated with improved survival.” About Candel Therapeutics Candel is a clinical stage biopharmaceutical company focused on developing off-the-shelf multimodal biological immunotherapies that elicit an individualized, systemic anti-tumor immune response to help patients fight cancer. Candel has established two clinical stage multimodal biological immunotherapy platforms based on novel, genetically modified adenovirus and herpes simplex virus (HSV) gene constructs, respectively. CAN-2409 is the lead product candidate from the adenovirus platform and is currently in ongoing clinical trials in non-small cell lung cancer (NSCLC) (phase 2), borderline resectable PDAC (phase 2), and localized, non-metastatic prostate cancer (phase 2 and phase 3). CAN-3110 is the lead product candidate from the HSV platform and is currently in an ongoing investigator-sponsored phase 1 clinical trial in recurrent high-grade glioma (rHGG). Finally, Candel’s enLIGHTEN™ Discovery Platform is a systematic, iterative HSV-based discovery platform leveraging human biology and advanced analytics to create new viral immunotherapies for solid tumors. For more information about Candel, visit: www.candeltx.com About the Phase 2 Clinical Trial of CAN-2409 in Non-Metastatic Pancreatic Cancer This randomized, open-label phase 2 clinical trial is designed to evaluate the safety, preliminary efficacy, and biologic activity of a 2-3 injection regimen of CAN-2409 plus prodrug (valacyclovir or acyclovir) in patients with borderline resectable PDAC who are being treated with neoadjuvant chemoradiation prior to resection. After a protocol amendment in 2022, when enrollment of patients with locally advanced PDAC was discontinued, the clinical trial was designed to exclusively focused on borderline resectable disease. The clinical trial remains active but is not currently unrolling new patients. In a previously completed phase 1b clinical trial, a highly significant increase in the number of CD8+ tumor infiltration lymphocytes was demonstrated at the site of the tumor after CAN-2409 treatment. About CAN-2409 CAN-2409, Candel’s most advanced multimodal biological immunotherapy candidate, is an investigational off-the-shelf replication-defective adenovirus designed to deliver the herpes simplex virus thymidine kinase (HSV-tk) gene to a patient’s specific tumor and induce an individualized, systemic immune response against the disease. HSV-tk is an enzyme that locally converts orally administered valacyclovir into a toxic metabolite that kills nearby cancer cells. Together this regimen is designed to induce an individualized and specific CD8+ T cell mediated response against the injected tumor and uninjected distant metastases for broad anti-tumor activity, based on in situ vaccination against a variety of tumor antigens. Because of its versatility, CAN-2409 has the potential to treat a broad range of solid tumors. Encouraging monotherapy activity as well as combination activity with standard of care radiotherapy, surgery, chemotherapy, and immune checkpoint inhibitors have previously been shown in several preclinical and clinical settings. Furthermore, to date, more than 1,000 patients have been dosed with CAN-2409 with a favorable tolerability profile to date, supporting the potential for combination with other therapeutic strategies without inordinate concern of overlapping adverse events. Currently, Candel is evaluating the effects of treatment with CAN-2409 in NSCLC, borderline resectable PDAC, and localized, non-metastatic prostate cancer in ongoing clinical trials. CAN-2409, plus prodrug (valacyclovir), has been granted Fast Track Designation by the FDA for treatment of PDAC or stage III/IV NSCLC in patients who are resistant to first line PD-(L)1 inhibitor therapy and who do not have activating molecular driver mutations or have progressed on directed molecular therapy. The Company’s pivotal phase 3 clinical trial in prostate cancer is being conducted under a Special Protocol Assessment by FDA. About Pancreatic Ductal Adenocarcinoma (PDAC) Pancreatic cancer is a highly lethal malignancy, and is the fourth leading cause of cancer-related death in the United States among both men and women. Based on the National Cancer Institute, Surveillance, Epidemiology and End Results (SEER) database, pancreatic cancer is expected to account for 3.3% of all new cancer cases with an estimated 64,050 new cases and estimated 50,550 deaths in 2023. Effective therapeutics for pancreatic cancer, including PDAC, which accounts for 90% of all pancreatic carcinomas, are urgently needed. Surgical resection offers the only chance of cure, thus a major therapeutic goal for subjects with non-metastatic disease is to achieve complete tumor resection. Surgical treatment (pancreaticoduodenectomy, also known as the Whipple procedure) or total or distal pancreatectomy (depending on tumor location) is generally the recommended treatment for patients diagnosed with resectable cancer; the addition of adjuvant chemotherapy has been shown to only slightly improve survival rates (20 to 23 months). To this end, there has been increasing use of neoadjuvant chemotherapy and chemoradiation regimens for subjects with borderline resectable pancreatic ductal adenocarcinoma. Neoadjuvant regimens are intended to debulk the tumor, thereby increasing the proportion of patients who may become eligible for surgical resection and achieve complete resection (i.e., resection with negative margins, designated ‘R0 resection’). Unfortunately, even when an R0 resection is initially achieved, cures remain elusive as most patients experience disease recurrence due to residual micrometastatic disease. In a recent meta-analysis of 20 studies representing 283 patients with borderline resectable PDAC, neoadjuvant FOLFIRINOX with or without radiotherapy, median overall survival was only 22.2 months (95% CI, 18.8 to 25.6 months). Immunotherapy with PD-1 antibodies with or without CTLA-4 antibodies has been uniformly unsuccessful in patients with PDAC due to the dense stroma that surrounds PDAC tissue and the absence of tumor infiltrating lymphocytes. Forward-Looking Statements This press release includes certain disclosures that contain “forward-looking statements,” within the meaning of the Private Securities Litigation Reform Act of 1995, as amended, including, without limitation, express or implied statements regarding the timing and advancement of development programs, including the timing and availability of additional data, key data readout milestones, and expectations regarding the therapeutic benefit of the Company’s programs, including the potential for its programs to extend patient survival. The words “may,” “will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,” “project,” “potential,” “continue,” “target” and similar expressions are intended to identify forward-looking statements, although not all forward-looking statements contain these identifying words. Any forward-looking statements in this press release are based on management’s current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-looking statements contained in this press release, including, without limitation, those risks and uncertainties related to the timing and advancement of development programs; the Company’s ability to continue as a going concern; expectations regarding the therapeutics benefit of the Company’s programs; that final data from the Company’s pre-clinical studies and completed clinical trials may differ materially from reported interim data from ongoing studies and trials; the Company’s ability to efficiently discover and develop product candidates; the Company’s ability to obtain and maintain regulatory approval of product candidates; the Company’s ability to maintain its intellectual property; the implementation of the Company’s business model, including strategic plans for the Company’s business and product candidates, and other risks identified in the Company’s filings, with the U.S. Securities and Exchange Commission (SEC) including the Company’s most recent Annual Report on Form 10-K filed with the SEC, and subsequent filings with the SEC. The Company cautions you not to place undue reliance on any forward-looking statements, which speak only as of the date they are made. The Company disclaims any obligation to publicly update or revise any such statements to reflect any change in expectations or in events, conditions, or circumstances on which any such statements may be based, or that may affect the likelihood that actual results will differ from those set forth in the forward-looking statements. Any forward-looking statements contained in this press release represent the Company’s views only as of the date hereof and should not be relied upon as representing its views as of any subsequent date. Investor ContactTheodore Jenkins VP Investor Relations and Business Development Candel Therapeutics, Inc.Tjenkins@candeltx.com Media ContactAljanae ReynoldsDirectorWheelhouse Life Science Advisorsareynolds@wheelhouselsa.com