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Systemic administration of the hyaluronidase - expressing oncolytic adenovirus VCN - 01 in patients with advanced or metastatic pancreatic cancer: first - in - human clinical trial R . Garcia - Carbonero 1 , M . Gil Martín 2 , R . Alvarez Gallego 3 , T . Macarulla Mercade 4 , M . C . Riesco Martinez 1 , C . Guillen - Ponce 5 , N . Vidal 6 , F . X . Real 7 , R . Moreno 8 , V . Maliandi 9 , A . Mato - Berciano 9 , M . Bazan - Peregrino 9 , G . Capella 2 , R . Alemany 8 , E . Blasi 9 , C . Blasco 9 , M . Cascallo 9 , R . Salazar 2 1 Medical Oncology, University Hospital 12 De Octubre, Madrid, Spain, 2 Medical Oncology, ICO - Institut Catala d'Oncologia Hospital Duran i Reynals , Hospitalet de Llobregat, Spain, 3 Medical Oncology, Hospital Madrid Norte San Chinarro Centro Integral Oncologico Clara Campal, Madrid, Spain, 4 Medical Oncology, Vall d'Hebron Institute of Oncology (VHIO) - Cellex Center, Barcelona, Spain, 5 Medical Oncology Department , Hospital Universitario Ramon y Cajal, Madrid, Spain, 6 Pathology, Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain, 7 Molecular Oncology Programme , Centro Nacional de Investigaciones Oncologicas (CNIO), Madrid, Spain, 8 LRT 1 /Procure, Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain, 9 VCN Biosciences , Sant Cugat del Valles, Spain . INTRODUCTION • Dense stroma is a hallmark of Pancreatic ductal adenocarcinoma (PDAC), which acts as a barrier for drug delivery . Targeting the components of the stromal compartment is a relevant approach for this tumor type . • VCN - 01 ( Rodriguez - Garcia, et al . Clin Cancer Res . 2015 ; 21 ( 6 ) : 1406 - 18 ) is a genetically modified oncolytic adenovirus that selectively replicates within tumor cells that have a deregulation of pRB pathway and not in normal cells and expresses PH - 20 hyaluronidase . • Activity of VCN - 01 is based on selective killing of tumor cells, which results in self - amplification and spread through the tumor mass, and the expression of hyaluronidase that partially degrades the extracellular matrix of the tumor . Such effect enhances gemcitabine uptake and induces potent immunomodulatory signals that could help recruit CD 8 + T cells . OBJECTIVE This is a First - in - human study (NCT 02045602 ) to investigate the safety, efficacy and pharmacodynamic profile of VCN - 01 after systemic administration alone or in combination with gemcitabine/nab - paclitaxel in patients with PDAC . METHODS NCT 02045602 is an open - label, dose - escalation study with three independent parts in patients with advanced cancer not amenable for curative treatment (Part I) or with advanced pancreatic adenocarcinoma to be treated with nab - paclitaxel / gemcitabine (Part II & III) . Results for Part I are not presented in this poster Primary Endpoints : • The safety & tolerability and determination of the RP 2 D of systemic of VCN - 01 combined with two regimens of nab - paclitaxel / gemcitabine were assessed through a dose - escalation schedule . Secondary Endpoints : • Presence of VCN - 01 in tumor biopsies at day 8 or day 28 . • VCN - 01 pharmacokinetics & shedding of VCN - 01 in blood and other fluids • Tumor response assessed according to RECIST v 1 . 1 . Exploratory Endpoints : • Assessment of PD biomarkers, such as hyaluronidase and immunological markers . CONCLUSIONS VCN - 01 shows a good safety profile when administered systemically in combination with the standard of care for pancreatic cancer, specially when delaying by 1 week the treatment with GE/nab - paclitaxel . Systemic VCN - 01 reaches pancreatic tumors and converts them from immunological deserts into CD 8 - infiltrated IDO - expressing tumors (marker of IFN - g mediated inflammation) . In addition VCN - 01 induces intratumor PD - 1 /PD - L 1 up - regulation in a subset of patients . All these changes result in evidences of clinical activity with both dosing regimens . FUNDING AND DISCLOSURE MBP, SM, EB and MC were funded by CDTI (PANCATHER project IDI - 20130759 ) . MBP, AMB, SM, MVM, EB, CB and MC are employees and RA is consultant in VCN Biosciences . MC and RA are co - inventors of one patent application concerning the expression of hyaluronidase by oncolytic adenoviruses and both have ownership interest in VCN Biosciences . Correspondence should be addressed to : Rocio Garcia - Carbonero , MD, DPhil, rgcarbonero@gmail . com METHODS CONTINUED Eligibility Criteria included the selection of patients with levels of neutralizing antibodies against adenovirus < 1 / 350 dilution at the moment of inclusion in the study Fig 1. NCT02045602 Study Design in three parts. Only data from Part II and III are shown in this poster RESULTS RESULTS CONTINUED Table 2. Treatment related Adverse Effects in each Part of the study VCN - 01 Pharmacokinetics & Pharmacodynamics Fig 3. Hyaluronidase quantification by ELISA in sera indicates a time - dependent increase of the protein consistent with VCN - 01 replication Clinical Activity Table 3. Efficacy Results by RECIST v1.1 Part III (VCN - 01 + GE/ nab - paclitaxel delayed) Part II (VCN - 01 + GE/ nab - paclitaxel) Table 4. Viral genome content in tumor biopsies (qPCR analysis) evidences VCN - 01 ability to reach tumors after systemic administration Fig 5 VCN - 01 protein positivity in tumor nuclei (by IHC) confirms viral replication adjacent to areas with CD8 infiltration and inflammation Fig 6 . IHC of immune markers in tumor biopsies confirms that VCN - 01 provokes CD 8 + - infiltration, IDO up - regulation and PD - 1 modulation in some patients . (A) Primary pancreatic tumor biopsy from patient 001 - 003 - 002 ; Part II ; (B) Hepatic metastasis from patient 001 - 005 - 002 ; Part III . Table 5. Summary of immune markers variations by IHC Part II Part III A. B. ESMO 2019 Congress, Barcelona, Spain Table 1 Patient Demographics for Part II and Part III Part II Part III Part II Part III Figure 4. Tumor burden analysis shows the presence of delayed responses suggestive of an immune - mediated mechanism of action Fig 2. Viral genomes in blood at different times after administration indicates the presence of secondary peaks suggestive of replication E1A nuclear staining