The Needle Issue #24


Welcome to The Needle, a newsletter from Haystack Science to help you navigate the latest translational research, with a roundup of the latest news on preclinical biotech startups from around the world.

The outlook for exits continues to improve, with SpyGlass Pharma ($172.5 million), Veradermics ($294.8 million), and Galecto ($316.3 million) all going public. Even less conventional biotechs like BioRestorative (a developer of adult stem cell therapies for bone disease, metabolic disorders and cosmetics) got out for $5 million, as well as the reappearance of a lesser-spotted preclinical SPAC. Preclinical financings ticked over with funding for a mixed bag of technologies, including exosomes, molecular glues, CAR-T therapies, peptides and antibody–oligonucleotide conjugates. The banner deal of recent weeks was Eli Lilly’s $2.4 billion acquisition of circular mRNA/LNP in vivo CAR-T developer Orna. We also witnessed a gaggle of deals for peptide therapeutics and shuttles to traverse the blood–brain barrier. As usual, anything we missed in the biotech startup world, let us know (info@haystacksci.com).

Haystack chat

X-ray crystallography has long been the go-to workhorse for providing atomic structures of drugs interacting with their protein targets. Increasingly, those static snapshots are being complemented by readouts from experimental analytical tools based on nucleic magnetic resonance (NMR) spectroscopy and cryoelectron microscopy (cryo-EM), offering drug developers a broader window into proteins as dynamic, breathing molecules. This is spurring a raft of new service provider startups, including AIffinity (Brno-Medlánky, Czech Republic), NexMR (Zürich, Switzlerand), CryoCloud (Utrecht), and Intellicule (West Lafayette, IN), all of which aim to supply drug-discovery teams with state-of-the-art platforms providing structural data with rapid turnaround times and low cost.

As many of the most compelling ‘undruggable’ targets are renowned shape shifters — aggregation-prone proteins like Tau, amyloid precursor protein (APP) or huntingtin in neurodegenerative diseases, or transcription factors like P53, KRAS and c-MYC in oncology — a lot of therapeutic startup activity has recently focused around so-called ‘intrinsically disordered proteins’ (IDPs). The ability to attain markedly different conformations under different conditions allows IDPs not only to play moonlighting roles or serve as hubs in signaling networks, but also to localize into liquid- phase condensates (or membrane-less organelles — attributes that make them acutely sensitive to mutations that can compromise specificity and lead to nonspecific binding, resulting in toxicity and disease.

As IDPs frequently resist attack by conventional drug discovery approaches, a slew of startups has sprung up to try to go after this target class, many using new structural techniques. These include Peptone (London, UK), Dewpoint Therapeutics (Boston, MA), brainQR Therapeutics (Göttingen, Germany), and Kodiform Therapeutics (Oxford, UK). Just last month, Topos Bio secured a $10.5 million seed round to “tackle ‘undruggable’ proteins driving Alzheimer’s and cancer”. Dewpoint also just announced it has dosed its first patient in a phase 1/2a trial of its lead beta-catenin program in gastric cancer and elected its MYC development candidate to take forward.

An important postscript to the startup activity targeting undruggable IDPs is that more conventional ‘druggable’ target classes, like tyrosine kinases, may also represent a fruitful hunting ground for dynamic conformational states that may have been missed by traditional crystallographic approaches. Given that conventional drug targets have relatively well-trodden clinical and commercial development paths, they may also represent simpler starting points and testing grounds for commercial programs aiming to apply the new analytical approaches to support medicinal chemistry programs around validated targets.

In a paper recently published in Science, the team of Charalampos (Babis) Kalodimos at St. Jude Children’s Research Hospital use high-resolution NMR spectroscopy to gain structural insight into how SRC family tyrosine kinases (Src, Hck, and Lck) achieve processive phosphorylation of multisite substrates.

The SRC enzyme family is essential for rapid and coordinated signaling in processes such as cell migration and T-cell activation. In addition, SRC family kinases are frequently overexpressed in tumors, contributing to the activation not only of multiple scaffold or signaling proteins, such as receptor tyrosine kinases (e.g., EGFR, FGFR, PDGFR or IGF1R), but also of downstream effectors (e.g., MAPKs, FAK, paxillin, p130Cas, ELMO1 and RAC1). Although there are approved drugs like the multikinase inhibitor Sprycel (dasatinib) that bind the SRC active site, these drugs have such extensive off-target and adverse side effects that there is a pressing need for new paths to more-selective SRC inhibitors.

SRC enzymes share a conserved domain organization, with a disordered N-tail, a tandem SH3–SH2 module, a kinase domain, and a disordered C-tail. All can carry out processive phosphorylation — a phenomenon where the enzyme phosphorylates multiple residues in a substrate during a single encounter. Each of these catalytic cycles typically requires ATP binding, phosphate transfer and ADP release, and ADP release is often the rate-limiting step. So, a question that has long puzzled structural biologists is how ADP-release–constrained kinases achieve sufficiently rapid turnover to successfully perform their function.

Using NMR spectroscopy with cryogenic probes — which reduce electronic/thermal noise and increase sensitivity up to five-fold compared with room-temperature probes — the St. Jude team characterized the conformational ensemble of the Src kinase domain and identified three interconverting states: a predominant active state, a previously described inactive Src/CDK-like state, and a hitherto unknown low-populated intermediate state positioned linearly between the other two. Structural determination revealed that this intermediate state displays features that are distinct from the active and inactive states. Its activation loop is partially folded, the P-loop is displaced inward, and the αC helix is shifted upward. This conformation binds ADP poorly relative to the active and inactive states, suggesting that it facilitates nucleotide release.

Using mutational analyses, the researchers then confirmed the functional importance of this intermediate state. Variants that eliminated this intermediate state while stabilizing the active state showed slower ADP dissociation, reduced catalytic turnover and impaired processive phosphorylation of the multisite Src substrate p130Cas. Instead of generating a fully phosphorylated substrate in a single binding event, these mutants accumulated partially phosphorylated intermediates. Equivalent mutations in other kinases of the SRC family, Lck and Hck, similarly reduced catalytic efficiency and impaired multisite phosphorylation of their respective physiological substrates CD3ζ and ELMO1 in Jurkat cells. Furthermore, these mutations compromised cellular functions measured via in vitro assays, including T-cell activation using Lck-deficient Jurkat cells and migration of mouse embryo fibroblasts lacking Src, Yes and Fyn in the presence of fibronectin. These molecular and functional findings indicate that the intermediate state is evolutionarily conserved and essential for processive activity across the SRC family.

Mechanistically, the work establishes that rapid ADP release, enabled by transient sampling of a structurally constrained intermediate, is critical for sustaining catalytic turnover rates that exceed the speed of substrate dissociation. More broadly, it shows that kinase conformational landscapes are tuned not only for switching between active and inactive states, but also for optimizing specific kinetic steps within the catalytic cycle.

From a drug developer’s standpoint, because Sprycel and other inhibitors target the active or inactive conformations of the SRC active site, the identification of a low-populated, functionally indispensable intermediate suggests a completely new strategy to target tyrosine kinases: selectively stabilize or destabilize the intermediate state to fine-tune catalytic turnover and processivity rather than simply blocking activity. Targeting such transient conformations could enable more precise modulation of signaling output, potentially improving selectivity and reducing off-target effects in kinase-directed therapies.

We look forward to seeing how many more of these intermediate states are uncovered in other kinase targets and whether pharmacological inhibitors targeting this state have advantages over orthosteric or allosteric chemotypes that conventionally have been used to inhibit the kinase active site or lock it in an inactive conformation. What is clear is that ultrafast NMR measurements of binding and state behavior are a powerful differentiating tool for understanding kinase activity where static structures aren’t enough.

Translational papers: Best of the rest

Target biology

E3 ubiquitin ligase TRIM21 enhances IL-17A signaling and drives autoimmune myocarditis by promoting TRAF3 lysosomal degradation in cardiac fibroblasts | PNAS

Systematic cysteine scanning identifies a druggable pocket in oncogenic KRAS | Cell Chemical Biology

Mutated FGFR1—the target for pemigatinib, erdafitinib and futibatinib in myeloid lymphoid neoplasms, urothelial carcinoma and cholangiocarcinoma, respectively—is also an oncogenic driver and therapeutic target in high-risk neuroblastoma | JCI

Targeting excessive cholesterol deposition alleviates secondary lymphoedema | Nature

Elovl6 inhibits colorectal cancer progression through stearic acid–mediated mitochondrial fusion and metabolic reprogramming | Science Advances

GCN5 drives MASLD progression through LXRα/SREBP1c signaling pathway–mediated de novo lipogenesis | Nature Communications

Liver exerkine reverses aging- and Alzheimer’s-related memory loss via vasculature in cell and mouse models of Alzheimer’s | Cell

GGC repeat expansions within new open reading frames are translated into toxic polyglycine proteins in oculopharyngodistal myopathy | Nature Genetics

Galectin-3 mediates lysosome-related inflammation within monocyte-derived macrophages in a mouse model of ischemic brain injury | JCI

RYK is a GPNMB receptor that drives MASH | Nature

Chaperone-mediated autophagy supports organ regeneration and fibroblast quiescence in mouse models of fibrosis | Science Translational Medicine

A GPX1-OSBPL8 axis mediates noncanonical in vivo ferroptosis and cancer growth suppression | Cell

R-loop processing via REXO4 exonuclease and RNaseH1 endonuclease plays role in genome instability and antitumor immunity, with REXO4 inhibitor suppressing tumor growth in melanoma mouse model | Science Advances

Immune checkpoint inhibitor–induced myocarditis is dependent on CD8 T cell–derived TNF and TNFR2 signaling | Journal of Experimental Medicine

Target validation

Genetic or pharmacologic blockade of parthanatos, genomic fragmentation by macrophage migration inhibitory factor (MIF) nuclease, reduces neuron loss and disease severity in autoimmune neuroinflammation | Nature Neuroscience

E3 ubiquitin ligase c-Cbl/Cbl-b antagonist inhibits EGFR turnover and sustains EGFR phosphorylation to enhance corneal re-epithelialization | PNAS

Structure-based design of an opioid receptor modulator for enhanced morphine analgesia | Science Advances

A reversible allosteric inhibitor of GlyT2 for neuropathic pain without on-target side effects | Nature Communications

Cotargeting DNA topoisomerase II enhances efficacy of RAS-targeted therapy in KRAS-mutant cancer models | JCI

Cancer immunotherapy

X-ray activated platinum complex induces DNA damage and enhances cancer immunotherapy through abscopal effect | Nature Biomedical Engineering

Single-cell screens identify ADAM12 as a fibroblast checkpoint impeding anti-tumor immunity | Cancer Cell

Flt3L-mediated tumor type 1 conventional dendritic cell expansion enhances immunotherapy by priming stem-like CD8+ T cells in lymph nodes | Nature Immunology

Ablation of prostaglandin E2 signalling through dual receptor knockout in CAR T cells enhances therapeutic efficacy in solid tumours | Nature Biomedical Engineering

Intravenous infusion of engineered megakaryocytes to produce oncolytic platelets reduces growth of mouse lung cancer models| PNAS

Antibodies that block SLAMF6 suppressor of T cell immunity inhibit receptor interactions in human T cells and boost survival in xenograft mouse models of T-cell lymphoma | Nature

The transcriptional repressor Fli1 inhibits proteostasis during nutrient stress to limit NK cell persistence in solid tumors | Immunity

Drug-controlled CAR T cells through the regulation of cell–cell interactions | Nature Chemical Biology

Lipid nanoparticle–mediated in vivo generation of panCAR immune cells for solid tumor immunotherapy | PNAS

Feasibility of rewiring STAT signaling from the cell surface with combinations of Interleukin-2, Interleukin-10, and Interleukin-21 ‘Trikine’ immunotherapeutics | Science Advances

Delivery, platforms, editing

Nebulized lipid nanoparticle delivery of mRNA as a GM-CSF replacement therapy for autoimmune pulmonary alveolar proteinosis | PNAS

High-throughput ligand diversification to discover chemical inducers of proximity | Nature Chemical Biology

Integration of ST2-RNA mitochondrial targeting sequence (RMTS) into sgRNA/Cas9 complex potentiates CRISPR editing of m.3243A>G mutant human cybrid cells and mouse cybrid xenograft models of mitochondrial diabetes mellitus|Cell Reports

Subretinally injected lipidoids derived from Coomassie brilliant blue bind and potentiate delivery of adenine base editing (ABE) ribonucleoproteins to the mouse retina|Nature Communications

High-throughput ligand diversification to discover chemical inducers of proximity | Nature Chemical Biology

Intrathecal dual AAV9-based base editing of Chd3 rescues behavioral abnormalities in mouse models of Snijders Blok–Campeau syndrome and transduces brain structures in non-human primates| Nature

Deep network hallucination for de novo design of ‘exoframe modulator’ peptides that bind transmembrane domains of dopamine D1 receptor to activate loss-of-function mutants| Nature

ISCro4 split-bridge RNA guided recombinase achieves ‘scarless’ deletion and inversion efficiencies >10% and insertion rates >6% for multi-kilobase DNA fragments at disease-relevant loci CNBP, CFTR and AAVS1 | Science

CRISPR-Cas13d-editing of RASGRP3 enables selective elimination of uveal melanoma cells | Molecular Therapy Oncology

Startup news

​It’s been a slow couple of weeks for news about early-stage biopharma venture funds. One bright spot from a strategic fund:

Denmark’s Gubra launches Gubra Ventures with Zoë Johnson leading new independent biotech company creation unit

Several announcements from governments seeking to boost biotech innovation:

India makes $11 billion investment in vaccines, antibody treatments, gene therapies, cell implants, insulin and recombinant protein drugs via Biopharma Strategy for Healthcare Advancement through Knowledge, Technology and Innovation (SHAKTI)

A UK Research & Innovation (UKRI) commissioned report explores relationships between UK universities and investors, highlighting Cambridge, Manchester, Newcastle, Queen’s University Belfast, Nottingham, Bristol, Leeds, and Oxford as hotspots

University of Cambridge, Oxford University, University of Manchester, University College London and Imperial College performed well compared with US powerhouses like Stanford University and MIT.

The UK report also underscores a finding from Haystack Science’s analysis of 2025 financing deals (Needle Issue #22) that most early-stage deals (pre-seed and seed financings) involve a unique group of investors:

A Pitchbook Report “Biopharma VC Trends” shows 2025 the lowest number of exits for biopharma private companies since before 2020.

At February’s ‘Insights to Impact’ event, Maryland’s TEDCO highlighted two biotechs as it Equity Growth Fund recipients:

Rise Therapeutics (food-grade probiotic firm developing Lactococcus lactis engineered to secrete anti-inflammatory surface layer protein A (SlpA) inserted into the bacteria’s thymidylate synthase (thyA) gene for containment for IBD)

Xcellon Biologics (CDMO for antibody-drug conjugates, providing end-to-end bioconjugation, process development, and GMP manufacturing)

Preclinical financings

Preclinical deals

Stay in touch

We hope you enjoyed this issue of The Needle and hit the button below to receive forthcoming issues into your inbox

If you’re interested in commercializing your science, get in touch. We can help you figure out the next steps for your startup’s translational research program and connect you with the right investor. Follow us on X, BlueSky and LinkedIn. Please send feedback; we’d love to hear from you (info@haystacksci.com).

Until next week,

Juan Carlos and Andy

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