By Claire Jeong, Chief Conference Officer, Vice President of Investor Research, Asia BD, LSN
Life Science Nation (LSN) is thrilled to announce the confirmed investors for RESI London 2025, taking place on December 4, at King’s Fund, 11 Cavendish Square, with virtual partnering on December 8–9. This premier event connects early-stage life science companies with a diverse array of global investors, facilitating meaningful partnerships and funding opportunities.
Meet the Confirmed Investors
RESI London 2025 will feature a robust lineup of investors spanning various sectors within the life sciences industry. Confirmed investors include:
This diverse group of investors represents a broad spectrum of interests, from pharmaceutical giants to specialized venture capital firms, ensuring that attendees have access to a wealth of expertise and potential funding sources.
Why Attend RESI London 2025?
RESI London 2025 provides an exceptional platform for early-stage companies to engage directly with top-tier investors across the life sciences industry, present innovations to a panel of esteemed judges in the Innovator’s Pitch Challenge (IPC), and receive valuable feedback. Attendees will have the opportunity to expand their network by building relationships with potential partners, collaborators, and industry experts, while also continuing discussions and meetings through virtual partnering on December 8–9, extending their reach and maximizing opportunities.
Whether you’re seeking funding, partnerships, or strategic alliances, RESI London 2025 provides the resources and connections necessary to propel your venture forward.
On September 24, uniQure reported 36-months positive topline data from the phase1/2 study of their candidate AMT-130 for the treatment of Huntington’s disease. AMT-130 consists of viral vector AAV5 and a synthetic miRNA that targets exon 1 of the huntingtin gene. The results showed that AMT-130, directly injected into the striatum at a dose of 6 x 10^13 genome copies per subject, slowed disease progression at 36 months, as measured by the composite Unified Huntington’s Disease Rating Scale and by Total Functional Capacity compared with a “propensity score-matched external control”.
The results have yet to appear in the peer-reviewed literature, and some experts have urged caution in their interpretation, particularly with regard to the use of external historical control groups and the small number of patients (12 have completed the 36-month period). However, uniQure’s data have been widely welcomed as a breakthrough for a field that has experienced its fair share of false starts (most recently Roche/Ionis halting of its phase 3 dosing of tominersen in 2021 after promising phase 1/2a results). Moreover, the findings have bolstered interest in therapeutic approaches targeting exon 1 in the mutant allele in addition to reducing levels of the full-length huntingtin protein.
Huntington’s disease is a triplet repeat disease in which the huntingtin gene’s exon 1 bears the CAG repeat encoding the polyglutamine stretch that defines the pathology. It’s therefore not surprising that the N-terminal part of HTT and its product have attracted attention as drug targets. Broadly speaking, scientists have tried to get at exon 1 in three ways: targeting the gene itself to block transcription, targeting the mutant mRNA to inhibit translation, and targeting the truncated protein that results from the mutant mRNA. A recent review provides a thorough survey of the preclinical work on these three fronts.
From the drug-discovery point of view, the most advanced programs focus on the development of ASOs or RNAi sequences against the CAG repeat in the mutant mRNA. The motivation behind this strategy is in part the realization that transcription of mutant HTTexon 1 results in a shortened 102 nt mRNA that encodes a toxic protein prone to aggregation: HTTexon1.
To explain what goes wrong in RNA splicing, we need to take a quick detour into the biochemistry of mRNA processing. In any cell, pre-mRNA processing is a competition between the splicing machinery (which removes introns from transcribed genes by recognizing an intronic 5′ splice site, branch point, and 3′ splice site) and the machinery that carries out intronic polyadenylation. Intronic polyadenylation cleaves transcripts within introns and adds a poly(A) tail to the shortened exon–intron fragment transcript when intronic sequences like AAUAAA are present together with a downstream U/GU-rich element.
All of the above is important for Huntington’s because, in healthy brains (specifically the striatum), U1 small nuclear ribonucleoprotein (snRNP) is thought to sit on the cryptic polyA sites in intron 1 of HTT, blocking intronic polyadenylation and enabling accurate splicing of introns and production of a full-length (9,500 nt) mature HTT mRNA. In contrast, in Huntington’s patients, increasingly long CAG repeats in the huntingtin pre-mRNA are thought to sequester U1 snRNP, thereby interfering with formation of the spliceosome complex and making cryptic polyA sites accessible. The result is premature termination of transcription within intron 1, resulting in the generation of the the shortened 120 nt HTTexon1 mRNA transcript that encodes an N-terminal 17-amino acid HTTexon1 protein.
In wild-type huntingtin, components of the spliceosome, such as U1 snRNP make cryptic polyA sites in intron 1 inaccessible to the transcriptional machinery. Accurate splicing ensues, and full-length huntingtin mRNA is produced. In Huntington’s Disease, the CAG repeat is thought to sequester U1 snRNP, exposing the cryptic polyA sites, ultimately leading to the production of HTTexon1. Source: Nature Communications)
Until the UniQure program, most disease-modifying therapies in the clinic have sought to downregulate full-length huntingtin and haven’t discriminated between mutant protein and wild-type protein. The prevailing thinking has been that going after full-length HTT makes sense because both the full-length protein—and fragments of it produced by proteolytic degradation—were likely the main problem.
By targeting exon 1, AMT-130 aims to specifically reduce production of toxic HTTexon1. And several other drug developers have also started to pivot and focus more closely on targeting HTTexon1, with the hope that such approaches might have greater efficacy in reducing huntingtin aggregate nucleation.
Just this year, Alnylam/Regeneron recently took ALN-HTT02 into phase 1b testing. This siRNA is conjugated to a 2′-O-hexadecyl C16 palmitate lipid that enables traversal of the blood brain barrier. It targets a conserved mRNA sequence within huntingtin exon 1, leading to the RISC-mediated degradation of all HTT mRNAs. The approach downregulates both HTTexon1 and full-length HTT — and does not discriminate between the wildtype and mutant alleles.
There are other molecules in development that directly target the expanded CAG repeat in exon 1 that are allele-specific. Vico Therapeutics’ VO659 is an ASO with an allele-preferential mechanism of action, targeting expanded CAG repeats in the mutant transcript and inhibiting translation of the mutant allele via steric block. It is currently in phase 1/2a clinical trials, and the company announced positive interim biomarker data in September 2024.
Meanwhile, in the preclinical space, Sangamo/Takeda are developing a mutant-allele selective approach, focusing on blocking transcription of the huntingtin gene using lentiviral vector delivered zinc finger repressor transcription factors (ZFP-TFs) that target the pathogenic CAG repeat. They have shown that their ZFP-TFs repress >99% of disease-causing alleles while preserving expression of normal alleles in patient-derived fibroblasts and neurons. Lentivirally delivered ZFP-TFs lead to functional improvements in mouse models, opening the door to their potential clinical development.
Haystack is aware of at least three other companies developing therapeutics aimed at reducing the toxic effect of HTTexon1, but details of their programs are scarce. China-based HuidaGene Therapeutics is developing a CRISPR-based gene editing product to fix the mutant allele. Galyan Bio was developing GLYN122, a small molecule directly targeting HTTexon1, but the company seems to have ceased operations. Similarly, Vybion has been developing INT41, a functional antibody fragment against HTTexon1, but its current status is also unclear.
It is sobering that over 150 years’ since the first description of Huntington’s disease, which many think of as the archetypal monogenic disease, that we still lack a definitive understanding of its pathogenic mechanism. We don’t know whether the pathology arises from HTT protein, RNA, DNA or some combination of these. And despite the buzz surrounding HTTexon1, most of the data supporting its relevance to human disease still originates from work in mouse models, which recapitulate only certain aspects of the human disorder. That said, raised levels of HTTexon1 are present in patient brain biopsies, with the longer CAG repeats in individuals with juvenile Huntington’s resulting in higher levels of the truncated transcript.
It will be exciting to follow the progress of UniQure’s AMT-130 as our understanding of where in disease progression, and in which patients, this therapy will be most effective. And beyond HTTexon1, other therapeutics targeting alternative disease pathogenic mechanisms are on the horizon. Last month, Skyhawk Therapeutics reported promising phase 1/2 clinical results for it oral small-molecule splice modifier SKY-0515. Elsewhere, broadening understanding of DNA mismatch repair enzymes and the role of somatic repeat instability in the disease have led to investment in a flurry of startup companies focused on this mechanism. That work is now leading to broader excitement that therapies may become available for other difficult-to-treat triplet repeat diseases like Fragile X syndrome, Myotonic dystrophy type 1 and Friedreich ataxia, as demonstrated by the recent deal between Harness Therapeutics and Ono Venture Investment.
Bilix, recognized as a top Innovator’s Pitch Challenge winner at RESI Boston this past September, is making waves in the biotech space with its innovative multi-modality approach to inflammatory and autoimmune diseases. In this interview, Myung Kim, Founder and CEO, shares how participating in RESI Boston helped the company connect with key investors, refine its strategy, and advance its clinical milestones.
Hear firsthand how Bilix is driving progress in complex disease treatment and discover how your company can join the next generation of innovators pitching at RESI London and RESI JPM. Applications are now open.
Commercial interest in targeted epigenetic therapies — agents that target specific genes without altering bases in their sequence or causing double-strand breaks or even single nicks in the DNA — continues to grow, as underscored by the latest financing announced by Epigenic Therapies. The unique selectivity and specificity of targeted epigenetic therapeutics offers compelling advantages over small-molecule epigenetic drugs, which target a specific epigenetic reader, writer or eraser, but affect genes across the genome and affect many diverse tissues, leading to narrow therapeutic windows that make them difficult to develop for conditions outside of cancer.
All of these therapies are designed around an alluring set of simple principles: take a gene-specific DNA-binding domain — zinc-finger proteins (ZFPs), ‘dead’ Cas9 (dCas9) with mutations in its RuvC and HNH endonuclease domains, or transcription activator-like effectors (TALEs) — and tether it via an amino acid linker to an enzymatic effector module. This effector is either an enzyme that directly places or removes a specific epigenetic modification (e.g., TET, histone demethylases or the histone acetyltransferase p300) or a transcriptional activator (e.g., VP16) or repressor (e.g., KRAB).
Epigenetic editing approaches have recently focused on dead CRISPR (dCRISPR) domains fused to various epigenetic effectors, but transcription activator-like effectors (TALEs) and zinc finger proteins (ZFPs) also continue to be explored. Source: TINS
A particularly compelling application for such treatments is genetic disorders of haploinsufficiency (like Dravet’s) or imprinting disorders (like Angelman’s or Prader Willi). There are also many of these diseases where the therapeutic genes would be too large (>4.0 kb) for a traditional AAV gene-therapy approach; in contrast, epigenetic editing machinery can be packaged into an AAV vector.
In a first paper published in Nature, the groups of Kevin Bender and Nadav Ahituv at UCSF (scientific co-founders of Regel Therapeutics) sought to test a targeted epigenetic therapy in patients with SCN2A mutations that exhibit decreased NaV1.2 function. These individuals have impaired action potentials, synaptic transmission and manifest diverse neurological symptoms and seizures, with few therapeutic options, beyond symptomatic anti-seizure medications that have a dizzying range of debilitating side effects.
The UCSF teams leveraged conditional genetic knock-in technolgoy or CRISPRa technology — an AAV-delivered SCN2A-promoter-targeting dCas9 fused to a VP16 activator domain — to upregulate transcription of the SCN2A gene. Using either approach, they were able to boost transcript levels from the healthy SCN2A allele, ameliorating electrophsiological deficits and chemical-induced seizure activity in Scn2a+/− mouse models. Importantly, these effects were seen in adolescent mice, which conventionally have been thought to be too old to respond to treatment. This suggests that rescue of normal dendritic excitability with epigenetic agents at later stages of life might be capable of restoring neuronal function, with implications for patients.
In a separate set of experiments, the authors showed that their epigenetic approach was able to rescue neurophysiological activity in haploinsufficient neuron-like cells from SCN2A-knockout human embryonic stem cells. This cross-species reproducibility provides further confidence that CRISPRa-mediated upregulation could be translated into human treatments.
In a second paper in Nature Biotechnology, a team from Epigenic Therapeutics (Shanghai, China) describes the design and validation of optimized epigenetic regulators (EpiRegs) to silence genes in a precise, durable way without altering genomic DNA. Epigen’s Shaoshai Mao and his collaborators at the Chinese Academy of Sciences and the First Affiliated Hospital of Anhui Medical University tested combinations of TALE- and dCas9-based systems, systematically optimizing effector domains and fusion architectures, looking for effective regulators of gene expression. The best-performing variant, EpiReg-T (a TALE-based system, which eliminates the need for a guide RNA), achieved 98% silencing of target genes in mice, substantially outperforming dCas9-based versions.
Using lipid nanoparticles (LNPs) for delivery, a single administration of EpiReg-T in macaques induced long-term repression of the PCSK9 gene, which encodes a validated target for the treatment of hypercholesterolemia. EpiReg-T reduced PCSK9 expression by >90% and LDL-cholesterol by about 60%, with effects persisting for nearly a year (343 days).
Mechanistically, the team used whole-genome bisulfite sequencing and cleavage under targets and tagmentation (CUT&Tag) to show that EpiReg-T induced stable DNA methylation and repressive histone marks at the PCSK9 promoter. The silencing persisted even after liver regeneration and could be reversed by targeted epigenetic activation. Multiomic analysis in mice, macaques and human hepatocytes confirmed high specificity of the manipulation and minimal off-target effects. Overall, these finding, as well as similar results reported in April by Chroma Medicine, establish epigenetic editing as a promising therapeutic platform for durable and reversible gene silencing.
Overall, targeted epigenetic therapies offer clear safety advantages over small molecules that indiscriminately target all genes under the control of an epigenetic eraser or writer enzymes. They avoid the potential risks associated with creating single- or double-strand DNA breaks associated with CRISPR/Cas9 gene, base or prime editing therapies. And they avoid the insertional mutagenesis risks associated with traditional viral gene therapies. What’s more, in applications requiring gene upregulation in haploinsufficient disease, these approaches maintain the endogenous regulatory context of the functional allele. This is in stark contrast to traditional gene-therapy replacement approaches, where overexpression of an introduced therapeutic gene can often lead to toxicities and immunogenecity.
Of course, questions still linger around the persistence of the changes elicited by these epigenetic agents. Will they persist in patients for long periods — for years or even decades? If they can, then epigenetic therapy may offer compliance advantages over small molecules, antibodies, ASOs or even siRNAs, which have treatment durations of six months or less.
Like all genetic medicines, though, delivery remains the key headache. Thus far, AAV vectors, lipid nanoparticles or ribonucleoproteins (RNP) have all been explored to deliver epigenetic therapies (with some evidence that RNPs might have advantages because they can result in higher dCas9 dosages within target cells). For AAV vectors, the fact that targeted epigenetic therapy might only need to be given once might be an advantage in terms of immunogenicity/neutralization concerns against the vector.
A broader point is that the safety profile of targeted epigenetic editors may offer advantages if AAV vectors are used as delivery vehicles: if the epigenetic agents themselves can be delivered at high dosage (given their intrinsic favorable safety profile and presumed maximal tolerated dose), perhaps AAV vector dosages could be lower than current practice. With many current gene therapies requiring dosages of 1013 or more viral particles/kg in patients, it is increasingly becoming clear that unacceptable liver toxicities arise from the virus at these levels in clinical studies. It will be interesting to follow this space as more agents enter human testing.
By Claire Jeong, Chief Conference Officer, Vice President of Investor Research, Asia BD, LSN
Life Science Nation (LSN) is excited to announce the lineup of investor panels at RESI JPM 2026, taking place January 12–13. These panels bring together leading venture capitalists, corporate investors, and strategic partners to discuss the latest trends, challenges, and opportunities in life science investing. From early-stage “first check” VCs to specialized sectors like Cell & Gene Therapy, AI in Healthcare, and Longevity, RESI JPM offers unparalleled insight into the funding landscape.
Day 1 – January 12
9:00 AM | “First Check” VCs Panel: Learn how early-stage investors evaluate founders, milestones, and the critical first institutional check.
10:00 AM | Medtech Strategics Panel: Explore how strategic investors from leading medtech companies drive growth through partnerships and acquisitions.
11:00 AM | Asia Cross Border Investments Panel: Sponsored by Enterprise Singapore, a RESI JPM Title Sponsor
1:00 PM | Family Offices Panel: Hear how family offices provide patient, mission-driven capital to early- and growth-stage companies.
2:00 PM | Cell & Gene Therapy Panel: Discover where capital is flowing in this transformative area of medicine.
3:00 PM | When Should Companies Exit Stealth Mode?: Gain insight into timing the transition from quiet development to public visibility.
4:00 PM | Aging and Longevity Panel: Learn how investors are deploying capital to solutions addressing the world’s aging population.
Day 2 – January 13
9:00 AM | Partnering with Global Pharma Panel: Understand how big pharma approaches early-stage partnerships and collaboration.
10:00 AM | Women’s Health Panel: Explore investment opportunities in an underserved market with enormous potential.
11:00 AM | AI in Healthcare: Discover how AI is reshaping drug development and care delivery.
1:00 PM | Orphan & Rare Diseases Panel: Learn about unique challenges and opportunities in niche, high-need markets.
2:00 PM | Corporate VC Panel: Hear how corporate venture capital balances strategic and financial goals to accelerate innovation.
3:00 PM | Techbio & Synthetic Biology Panel: Explore investment trends at the intersection of biology and technology.
4:00 PM | 2026 Outlook: VC Perspectives Panel: Gain insight into where investors see healthcare innovation heading in the coming year.
These panels are designed not only to share insights but also to foster dialogue between investors and innovators. If you are interested in speaking on a RESI JPM investor panel, please reach out here.
Registration for RESI JPM 2026 is now open, with Early Bird rates available until October 24. Don’t miss your chance to connect with top investors, strategic partners, and fellow innovators at one of the premier life science partnering events. Register for RESI JPM 2026
In this interview, Caitlin Dolegowski speaks with Cuong Do, Founder and Chairman of M6P Therapeutics, about the company’s groundbreaking lysosomal targeting platform, its applications in rare disease and oncology, and the experience of pitching at RESI Boston.
Caitlin Dolegowski (CD): M6P Therapeutics has achieved what was long thought impossible, delivering proteins to lysosomes. Can you explain the significance of this breakthrough?
Cuong Do (DO): An enzyme called GlcNac-1-phosphotransferase (PTase) is responsible for adding mannose 6-phosphate to the surface of lysosomal enzymes. People have tried and failed for decades to increase the expression of M6P, and everybody gave up. Our co-founder Stuart Kornfeld never gave up. He and his post-doc were able to engineer a variant of PTase that turned out to be 20X more effective than PTase itself in adding M6P to lysosomal enzymes. We built upon this breakthrough to create a platform that is able to create enzyme replacement therapies that have very high M6P content. Furthermore, our gene therapies are the only ones that result in M6P-containing enzymes being produced by the transduced cells.
We expanded upon the innovation and created chimeric antibodies that contain M6P as well. This allows these antibodies (after they bind to the targeted antigens) to be brought to lysosomes in virtually all cells in our bodies for degradation. This is a significant advantage over traditional antibodies relying on Fc clearance by only select immune cells.
CD: You have multiple rare pediatric drug designations and two programs nearing the clinic. What are the most exciting upcoming milestones for your pipeline?
DO: We are preparing to start an Investigator Initiated Trial in Australia for our M021 ERT for Pompe Disease in hopes of obtaining early human data demonstrating M021’s superiority over the standard of care.
CD: How does your lysosomal targeting platform extend beyond rare diseases, particularly in oncology with your chimeric PD-L1 and PD-1 antibodies?
DO: We figured out a way to add M6P to any protein, including antibodies. Our chimeric antibodies can be cleared by virtually all cells in the body since virtually all cells have receptors for M6P. This is especially effective for clearing surface antigens from cell surfaces. Our chimeric PD-L1 antibody is able to clear virtually all PD-L1 from the surface of tumor cells and thus activate T-cells and drive T-cell mediated tumor killing. Our chimeric version of Keytruda is able to remove PD-1 from the surface of T-cells and has shown to be more effective in inhibiting tumor growth in vivo than Keytruda itself.
CD: Can you walk us through your IP position and how it supports your growth strategy?
DO: We have invested heavily in IP that has created a portfolio of 9 patent families, 9 issued patents, and ~20 still in prosecution.
CD: Where are you in your fundraising journey, and what types of investors or partners are you looking to engage with?
DO: We have raised ~$40 million in our Seed and A rounds, which we invested to get our programs to where they are today. We are trying to raise a $5 million bridge now in anticipation of a $50+ million Series B next year. In addition to investors, we want to engage with potential partners who might be interested in our molecules.
CD: How did participating in the Innovator’s Pitch Challenge at RESI Boston help advance your business development or investor connections?
DO: We met a few companies who might be interested in partnering on some of our molecules. We’re continuing the conversations.
IPC Applications are now open for the next Innovator’s Pitch Challenge at RESI London 2025 and RESI JPM 2026, with spots filled on a rolling basis.
By Claire Jeong, Chief Conference Officer, Vice President of Investor Research, Asia BD, LSN
At RESI Boston September 2025, over 50 innovative companies participated in the Innovator’s Pitch Challenge (IPC), providing early-stage life science and healthcare companies with a unique platform to present their technologies and connect with potential investors.
The IPC finalists delivered 6-minute pitches followed by a 7-minute interactive Q&A session with a panel of investor judges. Each participating company also showcased its technology at a personalized table space in the RESI Exhibition Hall, creating additional opportunities for engagement.
A distinctive feature of the Innovator’s Pitch Challenge is its voting system. Registered RESI attendees—including startup executives, early-stage investors, and industry experts— “invested” in their favorite IPC companies using RESI cash provided at check-in. Attendees base their decisions on both the pitch presentations, the companies’ responses during Q&A, meeting with them in the exhibition hall at their table space, and during partnering or ad-hoc meetings at RESI.
Applications are now open for the next Innovator’s Pitch Challenge at RESI London 2025 and RESI JPM 2026, with spots filled on a rolling basis.
IsoTech Ltd is developing a novel wearable therapeutic medical device that stabilises blood pressure on standing to help older adults avoid dizziness and falls from orthostatic hypotension. The device guides a 30–60-second, on-demand isometric muscle contraction via a discreet retractable tether with visual and haptic cues, turning an evidence-based counter-manoeuvre into a simple, repeatable action without drug side effects. A completed proof-of-concept clinical study demonstrated clinically meaningful blood-pressure stabilisation in a substantial subset of patients with high usability and no unwanted adverse effects. The next phase is straightforward but execution-critical: design-for-manufacture and verification, Class I UKCA/CE technical documentation and light-touch QMS, tooling and pilot build, and a KOL-led seeded launch while preparing reimbursement pilots and strategic licensing options. Protected by patents on mechanism and form factor, ISO-101 aims to become the category-defining, real-time therapy for OH, improving independence for ageing populations and reducing falls-related costs for health systems at scale.
Dr Lochlainn Connolly, Founder – EVP Medical Affairs, Isotech | Dr Neil Fawkes, Founder / EVP R&D, Isotech | Dennis Ford, Founder and CEO, Life Science Nation | Iggy McGowan, Founder / CEO, Isotech
Bilix, founded in Oct 2018, raised $21 million in investments and received $3 million in government grants to develop a new drug for various inflammatory and autoimmune diseases. Our first target is ischemia-reperfusion injury, where unmet medical needs are high and no drugs. Global companies (Novartis, Roche, AstraZeneca, Argenx) are in Phase 2 or 3 trials with single-modality drugs (likely to fail). Our Phase 2a clinical trial (our drug being multi-modality, likely to succeed) runs from 2025.09 to 2026.08. We generate royalty revenue from Classys (a $3B market cap laser medical device company) through exclusive LO in cosmeceutical products. We are currently raising Series B-3 of $6M, of which $ 3 M has been secured. With $25.7 million pre-money valuation, an ROI of >10 times is achievable within three years through IPO/M&A. We can flip to a US company with vetted Series C investments from US/Foreign VCs.
Dennis Ford, Founder and CEO, Life Science Nation | Myung L. Kim, Ph.D., MBA, Founder and Chief Executive Officer, Bilix | Claire Jeong, CCO, VP of Investor Research, Asia BD, Life Science Nation
M6P Therapeutics focuses on lysosomes (the natural recycling center for cells) and has the only technology that can deliver any protein to lysosomes – a feat deemed impossible for over 50 years. The company has a deep pipeline, 6 rare pediatric drug designations, and an IP portfolio comprised of 9 patent families, 8 issued patents, and 20 in progress. Our Gaucher Disease ERT is ready for the clinic and our Pompe Disease ERT – which can restore and normalize muscle function – will be ready in 18 months. We also created a platform that can take any antigen-antibody complex to the lysosomes of any cell in the body (instead of relying on Fc clearance by select immune cells) for degradation. Our “chimeric” anti-PD-L1 antibody removes virtually all PD-L1 from the surface of tumor cells while our chimeric version of Keytruda is twice as potent.
Cole Van Vuren, Business Development Manager, Life Science Nation
The participating companies were grouped into 14 sector-focused sessions, with four companies per session. Each session was evaluated by a panel of judges, and the top-scoring companies were recognized for their strong pitches, ability to answer questions effectively, and clear communication of their value propositions.
Cuong Do
Dr Lochlainn Connolly, Founder – EVP Medical Affairs, Isotech | Dr Neil Fawkes, Founder / EVP R&D, Isotech | Dennis Ford, Founder and CEO, Life Science Nation | Iggy McGowan, Founder / CEO, Isotech
Dennis Ford, Founder and CEO, Life Science Nation | Myung L. Kim, Ph.D., MBA, Founder and Chief Executive Officer, Bilix | Claire Jeong, CCO, VP of Investor Research, Asia BD, Life Science Nation
Cole Van Vuren, Business Development Manager, Life Science Nation
