Posters and Guidelines
Thank you for considering to present your work as a poster at this conference. Please submit your poster abstract online within the advertised deadlines.
Poster preparation
- Page size: Page size is not important if you are presenting only digitally. However, if you are bringing along a hardcopy poster, print in A1 portrait format (presenters are responsible for printing their posters). Larger posters and those in landscape format may not be displayed due to space constraints. Do not laminate or print your posters on heavy printing paper.
- Naming your poster files: Name your poster files as follows: <your surname>-Oligo26-Poster.pdf, etc. For example, for David Jones, name your file as Jones-Oligo26-Poster.pdf. DO NOT name your poster files as, e.g., Oxford-poster, poster2026, Oxford-oligo-poster. Such files will not be accepted and you will be asked to resubmit a correctly named file.
- Poster submission: Submit your final poster as PDF files via the link below no later than 11th April 2025 Late posters may not be included in the conference programme. Please DO NOT send your poster or abstract files by email. Please ensure you send us the very final version of your poster (as well as your poster abstract), as once published, it cannot be replaced.
Before uploading your poster, you must make sure that you follow ALL of the instructions above!
Poster presentation:
There is no specific poster presentation session for digital or hardcopy posters. Submitted digital files of the posters will be offered online to the attendees, as well as displayed in the conference hall for those attending in-person. The presenters must bring a printed copy of their poster for display during the conference.
- Digital poster presentation: Digital/PDF posters will be made available via the secure conference documents page to the conference participants. The participants will be able to ask questions via the Zoom chatbox during the conference.
- Hardcopy poster presentation: If attending in-person, you may bring along a printed copy of your poster (maximum A1 portrait) to be displayed during the conference. You may be assigned a specific day to display your poster.
- Flash-talk videos (optional, but strongly encouraged): We are pleased to offer poster presenters the opportunity to prepare a short video presentation about their poster and send it before the conference. The videos will be made available on the LPMHealthcare YouTube channel. Below is further information for sending your video presentation.
- Download the opening slide (OligoOx26 flash talk first slide) and use it as the first slide of your presentation (see example: https://youtu.be/XatqenCd_IU?si=Yu1PooCD4JmSLAiz).
- Give your presentation (no longer than 5 minutes) using Zoom or another platform of your choice.
- Convert the video into a format compatible with YouTube (e.g., MP4).
- Send your video to OligoOxford@gmail.com using a file transfer program, such as MailBigFile or WeTransfer.
- The participants can post their questions on X at any time using the meeting hashtag #OligoOx26 – do tag @LPMHealthcare in your tweets.
Before uploading your poster, you must make sure that you follow ALL of the instructions above!
(Presenters in Bold)
Accepted poster abstracts (Unedited) will be published below. If your abstract has been accepted for presentation but it does not appear in the list below, please let us know as soon as possible by emailing OligoOxford@gmail.com.
Screening novel conjugated ASOs for efficacy and tissue specificity
Nina Ahlskog1, Ken Yamada2, Abinaya Ramesh1, David Coulson1, Thomas C Roberts1, Alyssa C Hill1, Jennifer Frommer1, Matthew J A Wood1
1Department of Paediatrics, Institute of Developmental and Regenerative Medicine (IDRM), University of Oxford, Oxford, UK.
2RNA Therapeutics Institute, University of Massachusetts Chan Medical School, Worcester, MA, USA.
Novel conjugation methods such as copper-free click-chemistry using e.g. bicyclo[6.1.0]nonyne (BCN) and extended nucleic acids (exNA) have enabled us to relatively quickly synthesize new ASOs at yields and purities suitable for in vivo testing. We utilized this to construct a library of ASOs targeting mouse Malat1 and injected them subcutaneously in C57BL/6 mice. We harvested tissues at different times following injection and assayed the efficacy in knocking down Malat1 RNA levels using qPCR. We hoped some of these novel compounds would have greater efficacy, lower toxicity, or extended bioavailability compared to the naked ASO. While many of our tested ASOs failed to perform better than naked ASO in targeting Malat1, a few conjugates stood out. As previously reported, lipid-conjugated compounds performed well in skeletal muscle. Interestingly, previously published for intracerebroventricular (ICV) administration, exNA-ASOs were very effective at reducing Malat1 RNA in CnS with subcutaneous administration while naked ASOs had no effect at all. In conclusion, we have shown that modifying the ASOs with conjugates or exNA can influence the delivery and efficacy of the ASO in specific tissues.
Sequence Specific Artificial Metallo-Nucleases
Eva Delahunt, Dr. Alex Gibney, Prof. Andrew Kellett. Dublin City University, School of Chemical Sciences, Dublin, Ireland
DNA damaging agents are clinically valuable therapeutics. Artificial Metallo-Nucleases (AMNs) are small molecules that cleave the phosphodiester backbone of DNA and offer an alternative method of DNA damage to existing therapies. The development of AMNs with sequence specificity is a promising strategy to curtail otherwise indiscriminate cellular oxidation. The synthesis of AMNs has become much more accessible in recent years by employing click chemistry in their preparation – a method recognised with a Nobel Prize. After functionalizing variable organic arms with alkynes, they can be clicked to central triazide mesitylene core to synthesise a bio-active C3 symmetric “Tri-Click” (TC) ligand which can chelate three copper ions. AMNs face a significant challenge in the form of macromolecular chelating agents, such as metallothioneins, that serve to prevent uncontrolled redox activity by labile metal ions. Consequently, AMNs with high stability, reactivity, and sequence specificity lie at the forefront of AMN design. Here we introduce Cu3-TC-Pico and Cu3-TC-PA, the first tridentate TC ligands. Sequence specificity was evaluated through DNA hairpin studies using Microscale Thermophoresis and Förster Resonance Energy Transfer melting analysis. Hairpin melting analysis showed destabilisation of the TA/TA step reflecting a perturbance of base-pairing. Gel electrophoresis experiments showed DNA damage at low micromolar concentrations, primarily through superoxide and hydrogen peroxide mediated mechanisms. Cu3-TC-Pico also displayed a hypochlorous acid mediated mechanism, which is uncommon with preexisting AMNs. In this work, Cu3-TC-Pico outperformed Cu3-TC-PA showing how small molecular derivatisation has a significant impact on the AMN activity profile.
Lesion induced DNA Amplification
Johanna Engelke1,2, Sabine Müller1
1Department of Biochemistry, University of Greifswald, Felix-Hausdorff-Straße 4, 17487 Greifswald,
2Department of Biochemistry, Christian-Albrechts-University of Kiel, Rudolf-Höber-Straße 1, 24118 Kiel, Germany
DNA amplification of nucleic acid biomarkers is fundamental for medical diagnostics. In low-resource settings, where temperature control and access to specialized equipment are often limited. A promising alternative for point-of-care diagnostics is lesion-induced DNA amplification (LIDA).LIDA is an isothermal amplification method that is based on the template-mediated ligation of DNA fragments. While classical LIDA uses enzymatic ligation, this project transfers the system into a non-enzymatic approach based on chemical ligation. The mechanism involves a cross-catalytic cycle in which the product strand from the first cycle serves as the template for the second cycle.Base mismatches are introduced to promote duplex dissociation, for reduced product inhibition and enhanced flexibility at the ligation site. Furthermore, the chemical reaction is carried out in a one-pot reaction. The aim of this project is to investigate the chemical ligation of DNA fragments in the first LIDA cycle and analyse and optimise ligation efficiency.
Base-modified hexitol nucleic acids for silencing a melanoma-specific long non-coding RNA
Yiyue Feng1,2, Eleonora Leucci3, Elisabetta Groaz1
1Rega Institute for Medical Research, Medicinal Chemistry, KU Leuven, Herestraat 49 Box 1041, 3000 Leuven, Belgium
2Rega Institute for Medical Research, Department of Microbiology, Immunology and Transplantation, KU Leuven, Herestraat 49 box 1043, 3000 Leuven, Belgium
3Laboratory for RNA Cancer Biology, Department of Oncology, KU Leuven, Leuven, Belgium
The abnormal expression of specific long non-coding RNAs (lncRNAs) has been associated with cancer and can be modulated using antisense oligonucleotides. However, conventional locked nucleic acid (LNA) gapmers are often associated with cytotoxicity and hepatotoxicity due to their strong hybridization affinity with RNA, encouraging the exploration of safer and more versatile chemistries. Here, we first evaluated a series of LNA gapmers to identify an effective target region within the survival-associated mitochondrial melanoma-specific oncogenic lncRNA SAMMSON. We then synthesized hexitol nucleic acid (HNA) phosphoramidites bearing both natural nucleobases and modified bases such as diaminopurine, 5-propynyl uracil, 5-propynyl cytosine, and G-clamp, and assembled them into SAMMSON targeting HNA gapmers. In cellular assays, a sequence with 10 HNA flanks and 6 DNA gap achieved measurable SAMMSON knockdown and exhibited reduced off-target effects compared to the corresponding LNA gapmer. Ongoing work focuses on nucleobase-modified HNA gapmers to further tune potency and selectivity, thereby advancing SAMMSON directed antisense agents for melanoma therapy.
Rational Design of an Acridine-derived Click Chemistry-based Artificial Metallo-Nuclease
Oliver Gould, Alex Gibney, Rebecca Lynn, Simon Poole, Bríonna McGorman, and Andrew Kellett.
Dublin City University, School of Chemical Sciences, Dublin, Ireland
Artificial metallo-nucleases (AMNs) are transition metal complexes capable of cleaving nucleic acids and represent a promising class of developmental therapeutics. We recently established that copper(I)-catalysed azide-alkyne cycloaddition (CuAAC) click chemistry offers a versatile approach for building new minor groove binding AMNs, epitomised by the Tri-Click (TC) class; here, three bidentate chelation sites comprising the N-triazole donor from the CuAAC reaction, together with the ‘clicked’ donor group, provide new ligand architectures that coordinate up to three bioactive copper(II) metal ions. Although the TC series are highly promising scaffolds, no method has yet been established to direct, or enhance, their DNA recognition properties. Herein, we report a new method for hybridising click chemistry-based AMNs with acridine, a potent DNA intercalating agent. Motivation for generating this conjugate stems from the opportunity to combine threading DNA intercalator properties; namely, DNA intercalation via the acridine unit, and minor groove cleavage affinity by the TC component. Two sites of the original TC scaffold were retained for CuAAC labelling with pyridine (Py) donors, thereby producing a Di-Click-Pyridine (DC-Py) unit, with the third site available for conjugation to the acridine (A) group. The resultant hybrid (DC-PyA), was then examined for its ability to coordinate copper(II) ions (Cu2-DC-PyA) with downstream direct and indirect DNA recognition properties, cleavage reactivity, and activity central to threading DNA intercalation observed.
Enhancing the Delivery of Antisense Oligonucleotides to the Heart, utilising Lipid Conjugates and Counterstrands
Muriel G Heitsch1,2, Dhanu Gupta1, Jennifer Frommer1
1Department of Paediatrics, University of Oxford, Old Road Campus, Oxford OX3 9DU, UK
2Department of Women’s and Children’s Health, Karolinska Institutet, Stockholm, Sweden
Uncurable inherited heart muscle diseases affect around 1 in every 250 people globally, presenting a significant public health burden. In recent years, antisense oligonucleotide (ASO) gene therapies, some of which use ASO gapmers, have emerged as potential treatments. ASO gapmers are short oligonucleotide sequences consisting of a central DNA region, with two flanking regions of RNA. Upon binding to the mRNA target, RNase H is recruited and degrades the bound mRNA, altering protein expression and thus potentially alleviating disease symptoms. Unfortunately, the in vivo delivery of ASOs remains a major challenge due to rapid clearance, limited tissue penetration, and inefficient cellular uptake. Whilst ribose sugar-modified and lipid-conjugated ASOs are known to increase delivery by increasing stability, biodistribution, and binding efficacy, efficient targeting of the heart remains difficult. We hypothesised that ASO uptake and subsequently efficacy in the heart could be improved by combining known lipid-conjugated and ribose sugar-modified gapmers with DNA counterstrands. To evaluate this, we assessed the impact on thermostability as well as the albumin binding properties of the ASOs, the latter indicative of an increased potential for greater biodistribution. Additionally, the overall performance of the ASO gapmers was investigated in vitro in both a human cardiomyocyte and a kidney cell line, providing information on performance in both the target tissue cell type and in a non-target tissue cell type. Together, the findings on ASO stability, albumin binding properties, and overall performance of lipid-conjugated and single- and double-stranded ASO gapmers provide us with an enhanced understanding of how to tailor ASO modalities towards the heart. Hence, this project constitutes an important step towards the development of an effective ASO therapy with enhanced cardiac delivery, driven by the interplay of conjugates and ASO structure.
Engineering Conjugated Antisense Oligonucleotides for Enhanced Cellular Uptake and Systemic Delivery
Ruhani Makkar, David Coulson, Muriel Heitsch, Nina Ahlskog, Rebecca Chalcraft, Matthew Wood, Jennifer Frommer
Department of Paediatrics, University of Oxford, Old Road Campus, Oxford OX3 9DU, UK
Antisense oligonucleotides (ASOs) are an emerging class of therapeutics that enable sequence-specific modulation of gene expression and offer tailored treatment strategies for genetic and neurological diseases. However, their clinical application is limited by inefficient systemic delivery and restricted transport across biological barriers such as the blood–brain barrier. Chemical conjugation strategies provide a promising approach to enhance cellular uptake, tissue specificity, and pharmacokinetic properties. In this project, ASOs were synthesized via solid-phase chemistry and functionalized post-synthetically using copper-free click chemistry, enabling scalable conjugation while avoiding cytotoxic copper reagents. Modified carbohydrate moieties were introduced as targeting ligands, allowing generation of single- and multi-conjugated ASOs with high conjugation efficiency. In vitro gymnotic dose–response studies in HEK293T cells demonstrated enhanced target knockdown for triple-conjugated ASOs (up to 80%) compared to single conjugates (~50%), indicating that increased ligand density improves functional activity. The triple-conjugated ASOs were tested in a human (hBEC-5i) and a rodent (bEND5) endothelial cell line to evaluate their performance. Both cell lines were included to assess potential species-dependent differences and enhance translational relevance. These findings support the development of optimized conjugation strategies to improve ASO delivery and guide future in vivo studies targeting BBB transport and systemic distribution.
Tuneable Ruthenium(II) Complexes for Targeted DNA Binding and Cleavage in Photodynamic Therapy
Stefania Scurtu1, Anna Ziemele1, Sebastian Golojuch2, Brionna McGorman1, Georgia Menounou1, Afaf H El-Sagheer2,3, Tom Brown2, Andrew Kellett1
1School of Chemical Sciences, Dublin City University, Glasnevin, Dublin, D09 K20V, Ireland.
2Department of Chemistry, University of Oxford, Oxford, OX1 3TA, United Kingdom.
3School of Chemistry & Chemical Engineering, Institute for Life Sciences, University of Southampton, Southampton, SO17 1BJ, United Kingdom.
The binding of small molecule metallodrugs to discrete regions of nucleic acids remains a powerful strategy in anticancer drug development, where interaction mode and sequence selectivity directly influence therapeutic outcome. Ruthenium(II) polypyridyl complexes, particularly, those incorporating the strongly intercalating dipyridophenazine (dppz) ligand, have gained considerable attention as next-generation photoactivated therapeutic agents due to their tuneable interactions with dsDNA and site mismatch recognition. Upon intercalation of the dppz core, the characteristic “DNA light-switch” luminescence response is produced, providing a direct photophysical signature of duplex binding. Subsequent activation with visible light generates reactive oxygen species (ROS), promoting direct photoinduced oxidative damage of oncogenes. Beyond DNA recognition, Ru(II)-dppz inorganic scaffolds function as effective photosensitisers in photodynamic therapy where off-target damage is minimised through spatiotemporal precision, confining toxicity to illuminated tumour regions. Herein, we report the biological evaluation of a novel series of tris-heteroleptic Ruthenium(II) complexes designed to modulate DNA affinity, duplex perturbation, and cellular toxicity profiles through rational modification of ancillary polypyridyl ligands including 1,10-phenanthroline (phen), 2,2’-bipyridine (bpy), dipyridoquinoxaline (dpq), 4,7-diphenyl-1,10-phenanthroline (dip), and 2,2’-biquinoline (biq) while retaining the dppz intercalative core. Biophysical studies confirmed strong intercalative dsDNA binding across the series, with characteristic hypochromicity, “light-switch” fluorescence enhancement, and apparent binding constants on the order of 10⁶ M⁻¹. Thiazole orange displacement and circular dichroism measurements supported high-affinity intercalation, while Topoisomerase I assays demonstrated plasmid unwinding consistent with helix lengthening induced by duplex insertion. Upon photoirradiation at 450 nm, the DNA-bound complexes induced efficient strand scission at sub-micromolar concentrations, converting supercoiled plasmid DNA to open-circular and linear forms. Reactive oxygen species scavenging revealed contributions from both Type I and Type II photophysical pathways, with ancillary ligand identity influencing oxidative pathway balance. Notably, complexes bearing dpq and dip ligands exhibited the highest DNA affinity, most efficient light-induced strand cleavage across the series, and sub-micromolar cellular IC50 values. In human breast cancer cell lines, the complexes accumulated in the nucleus, mitochondria and lysosomes, exhibiting pronounced light-dependent cytotoxicity with minimal dark toxicity, consistent with efficient ROS generation, loss of mitochondrial membrane potential, and lysosomal acidification. Collectively, these findings demonstrate the versatility of the ruthenium(II)–dppz scaffold as a tunable platform for controlled photoactivated cleavage. Ongoing work explores bioorthogonal click conjugation of these complexes to TFO and ASO platforms to enable sequence-directed photoactivation, potentially enhancing intracellular trafficking and endosomal escape.
