$TWST Twist just launched Express Screening Antibodies, a new high-throughput, cell-free service built to help solve a major wet-lab bottleneck for AI drug discovery. AI models can design thousands of antibody sequences in seconds, but testing them in the real world is slow. Previously, researchers had to either order raw DNA (in 4 to 7 days) and run their own cell transfections in-house, or wait 2 to 4 weeks for Twist's living mammalian cell (HEK293/CHO) expression workflows. This new launch builds a fast, automated "middle tier" between raw DNA and full mammalian production. Key highlights: • 5-Day Turnaround: Powered by LenioBio's ALiCE cell-free eukaryotic system, Twist converts digital sequences directly into purified, functional antibodies (5 to 20 µg of full-length IgG, scFv-Fc, or VHH-Fc) starting in just 5 business days. • Built for AI Scale: Engineered to match the massive output of generative AI models, allowing researchers to physically test thousands of antibody candidates per day. • Integrated Binding Data: Purified antibodies are routed straight into Surface Plasmon Resonance (SPR) assays to measure real-world target binding kinetics and affinity right on Day 5. Some context no how this fits into Twist's portfolio: • Synthetic DNA (Clonal/Express Genes): Delivers raw DNA in 4 to 7 days for teams running their own wet-lab expression. • Cell-Free Screening (New Express Screening Abs): Delivers µg-scale purified antibodies + SPR binding data in 5 days to rapidly triage massive AI sequence pools. • Mammalian Expression (HEK293/CHO): Delivers mg-scale purified protein in 10 to 25 days for deep characterization and pre-clinical lead selection. In short, Twist is giving AI biopharma teams a way to filter out non-binders and feed physical binding data back into their AI models in less than a week, before spending the time and money on full mammalian cell expression for their best candidates.

$PRME This guidance seems tailored to Prime's modular platform, even mentions "reverse transcriptase-based editors" twice 👀 Here are 4 key insights and why this could be a massive catalyst for Prime: 1) One BLA Across Mutational Families CBER's new blueprint outlines how companies can bundle multiple mutation-specific product variants for a single gene under one BLA, brand name, and NDC. Under the guidance, sponsors can establish an "Individualized Feature Space" (IFS). The core drug components (like the LNP delivery vehicle, formulation, and editor engine) stay fixed, while the guide sequences vary to address different patient mutations. • Instead of filing separate, costly BLAs for every individual mutation in a disease, the FDA would legally consider these variants to share the same active ingredient. • All variants could share a single brand name, prescribing label, and NDC (National Drug Code), with the container label simply specifying the targeted gene variant. 2) Adding New Mutations Post-Approval via In Vitro Data Alone Once an initial IFS is approved with clinical proof-of-concept, sponsors wouldn't need to run new clinical trials to add unstudied variants. • Under an approved Postapproval Change Management Protocol (PACMP), new mutation-specific guides could be added through streamlined CMC manufacturing supplements using in vitro potency and NGS off-target safety assays. • These in vitro safety packages could even be generated using scaled-down, representative material rather than full commercial batches. 3) Custom CMC and Process Validation (PPQ) Relief Prime editing pegRNAs vary in length and secondary structure depending on the mutation, which traditionally created major manufacturing validation headaches. • CBER explicitly addresses this, instructing sponsors to design flexible chromatography and mixing controls upfront rather than revalidating the process for every sequence. • Even better, the FDA removes the requirement to run Process Performance Qualification (PPQ) campaigns on every variant. Sponsors could bracket manufacturing scales instead. For Prime, managing a $108.8M cash balance as of Q2, avoiding redundant clinical trials and validation campaigns would preserve critical runway. 4) Commercial Blueprint for Wilson Disease and Beyond As mentioned, CBER explicitly cites "reverse transcriptase-based editors" (part of Prime's editing platform) in the text when defining "platform" boundaries. • In Wilson disease, Prime's lead in vivo asset (PM577a) targets the western H1069Q mutation, while a follow-on candidate targets the East Asian R778L mutation. Prime could clinically validate both under a shared ATP7B IFS, secure a single BLA, and then systematically roll out pegRNAs for the long tail of rare ATP7B mutations using in vitro data to capture the entire global market. • The exact same playbook applies to Prime's cystic fibrosis program (covering non-modulator CFTR mutations), PM647 in AATD (expanding from PiZ to rare SERPINA1 variants), and ex vivo CGD. Why is this all important? A major bear thesis on mutation-specific gene editing has always been commercial fragmentation. If a therapy only fixes one specific spelling mistake, how do you affordably treat the hundreds of other mutations in the same gene? This new draft guidance directly answers that question. Keep in mind that this framework applies to multiple mutations within a single target gene, so PM577a (Wilson) and PM647 (AATD) will still require separate BLAs despite sharing the same Universal Liver LNP. In summary, this draft guidance provides the exact regulatory bridge Prime would need to overcome mutation fragmentation and allow them to turn bespoke single-mutation fixes into scalable, single-license commercial franchises without having to fund standalone clinical trials for every variant.