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For decades, a medical puzzle has perplexed scientists: Why do cancers rarely arise in the heart? Despite its rich blood supply, both primary cardiac tumors and secondary metastases to the heart are exceedingly uncommon. Traditional explanations have focused largely on the biochemical microenvironment.Recently, Serena Zacchigna’s team at the University of Trieste published an online paper in Science titled “Mechanical load inhibits cancer growth in mouse and human hearts.” The study proposes an entirely new physical explanation: the mechanical forces generated by the heart’s continuous, rhythmic contractions themselves constitute a powerful anti-cancer barrier.Using an in vivo gene-editing model, the researchers directly demonstrated the heart’s innate resistance to malignant transformation. They intravenously injected an AAV9 virus expressing Cre recombinase into seven LSL-K-RasG12D/+; p53f/f genetically engineered mice, thereby simultaneously activating the oncogenic K-Ras mutation and knocking out the tumor suppressor p53. Two months later, analyses showed comparable levels of genetic recombination in the liver, skeletal muscle, and heart. Multiple rhabdomyosarcomas developed in skeletal muscles of the limbs, trunk, and neck, yet no tumors formed in the heart. This finding directly overturns the notion that “the heart is spared simply because it never encounters oncogenic signals,” and instead demonstrates that the heart harbors an active defense mechanism that suppresses cancer cell proliferation.Cat.No.Product NamePriceAAV00020ZCre Adeno-associated virus(AAV Serotype 5)InquiryAAV00044ZCre Adeno-associated virus(AAV Serotype 1)InquiryAAV00045ZCre Adeno-associated virus(AAV Serotype 2)InquiryAAV00046ZCre Adeno-associated virus(AAV Serotype 6)InquiryAAV00047ZCre Adeno-associated virus(AAV Serotype 8)InquiryAAV00048ZCre Adeno-associated virus(AAV Serotype 9)InquiryAAV00319ZCMV-Cre AAV (Serotype Retrograde)InquiryAAV00322ZCAG-Cre AAV (Serotype Retrograde)InquiryAAV00327ZSyn-Cre AAV (Serotype Retrograde)InquiryAAV00333ZCAG-Cre AAV (Serotype BR1)InquiryAAV00504ZAAV5-hSyn-CreInquiryAAV00545ZCAG-Cre AAV (Serotype AAV-BI30)InquiryAD00299ZCre adenoviral particlesInquiryTo probe the role of mechanical forces, the team devised a clever “heterotopic heart transplantation” model: donor hearts were transplanted into the necks of recipient mice and connected to major vessels for blood supply, but because these hearts did not participate in systemic circulation, the left ventricle bore virtually no pumping load—i.e., they were “mechanically unloaded.” The results were striking: on these non-beating hearts, lung and colorectal cancer cells proliferated rapidly and formed tumors. By contrast, in normally contracting cardiac tissue, cancer cell growth was strongly inhibited. This observation was independently validated in engineered cardiac tissues where mechanical load can be precisely controlled.From physical force to genetic switch: unveiling a complete anti-cancer signaling pathwayHow are mechanical forces translated into biochemical instructions that suppress proliferation? Through spatial transcriptomics and related techniques, the study found that cancer cells within cardiac metastases exhibit a distinctive gene expression profile characterized by reduced chromatin compaction and increased openness—an epigenetic state associated with proliferation inhibition. Crucially, the researchers identified the “sensor” that links mechanical force to this state: the protein Nesprin-2. Located at the nuclear envelope, Nesprin-2 transmits mechanical stretch perceived in the cytoplasm to the nuclear interior.Decisive evidence came from knocking down Nesprin-2 in lung cancer cells and then implanting them into normally beating mouse hearts. These cells behaved as if they could no longer “feel” mechanical force; their chromatin failed to undergo the suppressive epigenetic changes and they formed large tumors. This provides elegant proof that Nesprin-2 is the core molecular switch converting the mechanical signals of cardiac contraction into anti-cancer instructions.Figure 1. Key mechanisms inhibiting cancer cell proliferation in the heart. (CIUCCI, Giulio, et al., 2026)This study not only offers a concise and elegant physical solution to the century-old mystery of why the heart rarely develops cancer, but also inaugurates a new paradigm of “mechanical oncology.” It demonstrates that mechanical signaling can directly regulate cellular epigenetic states and determine cell fate. The findings open revolutionary avenues for cancer therapy: Could we design drugs that mimic mechanical signals, or apply similar mechanical stimuli to other tissues to suppress tumor growth? The power of the heartbeat not only sustains life—it may also quietly protect it.ReferenceCIUCCI, Giulio, et al. Mechanical load inhibits cancer growth in mouse and human hearts. Science, 2026, 392.6796: eads9412.
In 2020, mRNA vaccines emerged as dark horses that reshaped the course of the COVID-19 pandemic. Now, this Nobel Prize–winning technology is turning its sights on cancer. Around the world, mRNA vaccines targeting solid tumors such as melanoma, small-cell lung cancer, and bladder cancer have entered clinical trials. In 2023 alone, nearly 20 million new cancer cases were reported globally, with more than 90% of cancer deaths attributable to the invasion and metastasis of solid tumors. Yet the central question has remained: how exactly do mRNA vaccines “teach” the immune system to recognize and eliminate cancer cells?According to conventional wisdom, a type of immune cell known as type 1 classical dendritic cells (cDC1) is the “gold-standard instructor” for activating CD8+ T cells. Whether in viral infections, tumor development, or conventional protein and DNA vaccines, cDC1 cells—thanks to their high-efficiency cross-presentation—are thought to shoulder most of the burden of activating CD8+ T cells with exogenous antigens. Do lipid nanoparticle (LNP)–encapsulated mRNA vaccines follow the same rule?A recent study published in Nature, titled “mRNA vaccines engage unconventional pathways in CD8+ T cell priming,” by scientists from Washington University School of Medicine and other institutions, provides a surprising answer: mRNA-LNP vaccines do not need to rely on the cDC1 “main highway” at all. Instead, they engage two redundant routes that involve both cDC1 and their “cousins,” cDC2.Cat.No.Product NamePricePMCRL-0016Sox2 circRNA-LNPInquiryPMCRL-0017Oct4 circRNA-LNPInquiryPMCRL-0018Klf circRNA-LNPInquiryPMmRNL-0001EGFP mRNA-LNPInquiryPMmRNL-0002mCherry mRNA-LNPInquiryPMmRNL-0003Firefly Luciferase mRNA-LNPInquiryPMmRNL-0004Cas9-HA mRNA-LNPInquiryPMmRNL-0005EGFP mRNA (no modificaiton)-LNPInquiryPMmRNL-0006mCherry mRNA (no modificaiton)-LNPInquiryPMmRNL-0007Firefly Luciferase mRNA (no modificaiton)-LNPInquiryPMmRNL-0008spCas9 mRNA (no modificaiton)-LNPInquiryPMmRNL-0009spCas9 mRNA (N1-Me-Pseudo UTP modified)-LNPInquiryPMmRNL-0010SARS COV-2 Spike Protein (Alpha Variant) mRNA-LNPInquiryIn mouse studies, the researchers found that even in the absence of cDC1 cells, mRNA cancer vaccines could still elicit robust anti-tumor T cell responses and successfully clear sarcomas—malignant tumors arising in connective tissues such as fat and muscle. This finding overturns textbook immunology, because cDC2 cells have traditionally been considered nonparticipants in CD8+ T cell responses induced by conventional vaccines. It also helps explain the exceptional potency of mRNA vaccines and points to clear targets for optimizing future cancer vaccine design.Using gene knockout mouse models, the team dissected the roles of different dendritic cell subsets and showed that mRNA-LNP vaccines recruit cDC1 and cDC2 in a redundant fashion. Even more intriguingly, although the T cells activated by each subset bear slightly different molecular “fingerprints,” both populations can drive effective anti-tumor responses and form immune memory. In other words, the immune system provides mRNA vaccines with a built-in “double insurance” mechanism—if one road is blocked, the other still works.Figure 1. CD8+ T cells activated by cDC2 cells are capable of exerting anti-tumor effects. (JO, Suin, et al., 2026)The researchers also uncovered a distinctive way that cDC2 cells activate T cells: cross-dressing. In simple terms, certain non-hematopoietic cells (such as tumor or stromal cells) first produce antigen proteins according to the mRNA instructions, process them into peptides, and display them on their own MHC-I molecules. These cells then transfer the peptide–MHC–bearing membrane complexes wholesale to cDC2 cells, which use this “ready-made evidence” to activate T cells. This process depends on type I interferon signaling and completely bypasses the WDFY4-dependent cross-presentation pathway typically used by cDC1. In other words, mRNA vaccines enable cDC2 to activate T cells using antigens “borrowed” from other cells.The implications go well beyond basic immunology. In the clinic, cancer patients’ responses to mRNA vaccines can vary substantially, potentially reflecting differences in the relative abundance or functional state of cDC1 and cDC2 within individuals. Since both routes can be effective, future vaccine designs need not “bet everything” on cDC1 alone; they can aim to co-activate both subsets and even harness cross-dressing to boost cDC2 presentation efficiency. As the researchers quipped, cDC1 are like full-time professors, while cDC2 are largely self-taught but capable teaching assistants—usually quiet, yet perfectly able to carry the day when it counts.This study was conducted in mouse models, and the human immune system is more complex. Even so, it opens a new window: the striking potential of mRNA vaccines in cancer therapy may stem from their willingness to “take the road less traveled,” mobilizing long-overlooked “bench players” in the immune system. For patients awaiting more effective treatments, this is an encouraging sign.ReferenceJO, Suin, et al. mRNA vaccines engage unconventional pathways in CD8+ T cell priming. Nature, 2026, 1-10.
The mechanisms underlying interactions between tumor cells and myeloid cells within the tumor microenvironment (TME) remain unclear, and predictive biomarkers for patient responses to myeloid checkpoint blockade therapy are lacking.Recently, a team led by Chengcheng Zhang at the University of Texas Southwestern Medical Center published a study online in Science Immunology titled “Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer.”The study identifies a specific interaction between tight junction proteins known as claudins (CLDNs) and leukocyte immunoglobulin-like receptor subfamily B members LILRB2 and LILRB5. Across multiple human cancer cohorts, the spatial proximity between LILRB2-positive macrophages and CLDN-expressing cancer cells correlates with clinical outcomes, highlighting the potential of this spatial relationship as a biomarker.Cat.No.Product NamePriceCSC-DC008707Panoply? Human LILRB2 Knockdown Stable Cell LineInquiryCSC-RO02453Monkey LILRB2 Stable Cell Line - CHOK1InquiryCSC-RO0584Monkey LILRB2 Stable Cell Line - HEK293TInquiryCSC-RO0622Human LILRB2 Stable Cell Line - MC38InquiryCSC-RO0623Human LILRB2 Stable Cell Line - CT26InquiryCSC-RO0663Human LILRB2 Stable Cell Line - 3A9InquiryCSC-RO0664Human LILRB2 Stable Cell Line - HEK293TInquiryCSC-RO0665Human LILRB2 Stable Cell Line - CHO-K1InquiryCSC-RO0931Human LILRB2 Stable Cell Line - THP-1InquiryCSC-SC008707Panoply? Human LILRB2 Over-expressing Stable Cell LineInquiryAD09180ZHuman LILRB2 adenoviral particlesInquiryLV17002Lhuman LILRB2 (NM_005874) lentivirus particlesInquiryLV17003Lhuman LILRB2 (NM_001080978) lentivirus particlesInquiryIn syngeneic LILRB2 transgenic and humanized mouse models, the interaction between CLDN18.2 and LILRB2 triggers bidirectional signaling that enhances the immunosuppressive activity of myeloid cells and accelerates tumor progression. These effects can be reversed by blocking LILRB2. The CLDN-LILRB2 axis maintains immunosuppression by regulating NF-κB and STAT signaling pathways. This study reveals a regulatory role of tight junction proteins in modulating myeloid cells within the tumor microenvironment and provides a theoretical basis for targeting this pathway in cancer therapy.T cell–based immune checkpoint blockade therapies are effective in some cancer patients, suggesting the existence of additional immune evasion mechanisms within the TME. Myeloid cells are often the most abundant immune cell population in the TME, where systemic and local signals can drive large numbers of these cells toward an immunosuppressive phenotype.These include monocytic and polymorphonuclear myeloid-derived suppressor cells (M-MDSCs and PMN-MDSCs), as well as specific subsets of macrophages, neutrophils, and dendritic cells. Therefore, targeting or reprogramming immunosuppressive myeloid cells represents a promising therapeutic strategy.Leukocyte immunoglobulin-like receptor subfamily B (LILRB) proteins are a class of type I transmembrane receptors containing immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and are expressed in hematopoietic cells. Upon ligand binding, LILRBs recruit Src homology 2 domain-containing phosphatases such as SHP-1, SHP-2, or SH2-containing inositol phosphatase (SHIP) to suppress immune activation. LILRBs are primate-specific, and their murine homologs, paired immunoglobulin-like receptor B (PirB) and glycoprotein 49B1 (gp49B1), differ in expression patterns and ligand recognition, limiting the utility of knockout mouse models for studying LILRB biology.Figure 1. The scheme of the interaction of CLDNs and LILRB2 regulates the immunosuppressive myeloid cells and cancer cell proliferation to promote cancer development. (LIU, Xiaoye, et al., 2026)Blocking signaling mediated by LILRB1, LILRB2, LILRB3, LILRB4, or leukocyte-associated immunoglobulin-like receptor 1 (LAIR1) in normal or malignant human immune cells enhances antitumor immune activation, establishing LILRBs as myeloid immune checkpoints. Several clinical trials have been initiated to evaluate the safety and efficacy of LILRB-based therapeutics. However, how LILRBs interact with cells in the tumor microenvironment to regulate tumor development remains unclear, and the characteristics of cancer patients who may benefit from LILRB2 blockade therapy are not yet defined.Claudins (CLDNs) specifically bind to LILRB2 and LILRB5, including aberrantly expressed CLDN18.2 found in gastric, pancreatic, and biliary cancers. In healthy individuals, CLDNs are expressed on epithelial and endothelial cells, but their expression is dysregulated in cancer cells. The receptors for CLDNs had previously not been clearly identified.This study demonstrates that CLDN18.2 activates LILRB2 signaling to sustain the immunosuppressive function of myeloid cells and promote tumor progression. LILRB2 mediates CLDN18.2-induced signaling in MIA PaCa-2 cells. The physical proximity between LILRB2-positive macrophages and CLDN-positive cancer cells is associated with poor therapeutic outcomes across five human cancer cohorts, revealing a clinically relevant CLDN-LILRB axis that regulates tumor progression.ReferenceLIU, Xiaoye, et al. Claudins interact with LILRB immune inhibitory receptors to promote myeloid immunosuppression in cancer. Science Immunology, 2026, 11.118: eadt7832.
Prime editing (PE) enables precise genetic modifications using canonical prime editing guide RNAs (pegRNAs), which append a reverse transcription template and primer binding site (RTT–PBS) to the 3’ end of a CRISPR-Cas guide RNA. Although delivery of PE ribonucleoproteins (RNPs) holds substantial therapeutic potential, their limited genome-editing activity constrains clinical applications.Recently, a team led by Chunqing Song at Westlake University, China, published a study in Nature Biomedical Engineering titled “Boosting prime editing with engineered non-canonical pegRNAs.”The study developed non-canonical pegRNAs (npegRNAs) that successfully overcome the bottleneck of transient-delivery efficiency in prime editing, markedly enhancing efficiency and stability without increasing off-target risk. These npegRNAs are especially well-suited to RNP and RNA delivery systems required for clinical translation.Gene-editing technologies, particularly those within the CRISPR–Cas toolkit, herald a new era of precision medicine and biological research by enabling targeted DNA modifications in mammalian cells. Prime editing is a subclass of CRISPR–Cas tools distinguished by its ability to enact accurate DNA changes without inducing double-strand breaks, offering a safer alternative for gene correction.These tools excel at a range of edits, including base substitutions, insertions, and deletions. The prime editing system operates with a fusion of Streptococcus pyogenes (Sp) Cas9 nickase (Cas9n) and a reverse transcriptase (RT), guided by a pegRNA—an extended single-guide RNA (sgRNA) bearing a 3’ RTT–PBS extension.Cat.No.Product NamePriceOVT2645pLX-sgRNAInquirySKO0017EZR Validated?sgRNA?vectorInquirySKO0026PAM Validated?sgRNA?vectorInquirySKO0208PITPNB Validated?sgRNA?vectorInquirySKO0292AES Validated?sgRNA?vectorInquirySKO0328BAX Validated?sgRNA?vectorInquirySKO0358CBS Validated?sgRNA?vectorInquirySKO0396CNP Validated?sgRNA?vectorInquirySKO0417CTTN Validated?sgRNA?vectorInquirySKO0659PCNT Validated?sgRNA?vectorInquirySKO0714PSCA Validated?sgRNA?vectorInquirySKO0742RHOC Validated?sgRNA?vectorInquiryOVT3065pLH-sgRNA1-2XMS2InquiryRecent efforts have aimed to improve efficiency by advancing core PE proteins—such as hyPE, PE2*, PEmax, PE6, and PE6d—and by incorporating DNA- or RNA-binding motifs, including the RNA-binding motif La fused in PE7. While pegRNAs specify the DNA target and encode the intended edit, their 3’ extensions are vulnerable to cellular exonucleases, compromising the integrity of the RTT–PBS that is critical for PE5.Figure 1. Design of npegRNAs that improves PE efficiency. (FANG, Guo-Qing, et al., 2026)Engineered pegRNAs (epegRNAs) provide nuclease resistance via added motifs such as evopreQ1 but inadvertently reduce Cas9 binding. A split pegRNA system, in which the sgRNA and RTT RNA function separately, demonstrates the feasibility of separating editing components, though it is generally less effective than canonical pegRNAs. Because of its transient activity, PE RNP delivery is theoretically effective and safe for in vivo genome editing, yet its practical efficiency remains low and lags behind DNA or mRNA delivery methods across various cell types, hindering the clinical use of PE for treating genetic diseases.Here, the researchers introduce structurally guided engineering of PE complexes using non-canonical pegRNAs (npegRNAs), integrating the RTT–PBS into sgRNA loops to enhance PE efficiency. This approach yields improved precise editing rates across diverse genomic loci and cell types and enhances therapeutic gene correction in a mouse model of tyrosinemia. Cas9-associated npegRNAs are more resistant to exonuclease degradation, potentially boosting the targeting efficiency of PE complexes in living cells.With PE RNP delivery, npegRNAs achieved on average a 26.8-fold higher editing yield than standard pegRNAs and a 5.9-fold increase over engineered pegRNAs (epegRNAs). Moreover, npegRNA-mediated RNPs increased the efficiency of installing disease-associated mutations by up to 123-fold in human cell lines, including Jurkat T cells and induced pluripotent stem cells. Collectively, these findings establish a potent PE strategy and highlight the therapeutic potential of npegRNAs in prime editing applications.ReferenceFANG, Guo-Qing, et al. Boosting prime editing with engineered non-canonical pegRNAs. Nature Biomedical Engineering, 2026, 1-14.
Chimeric antigen receptor T (CAR-T) cell therapy has emerged as a breakthrough in cancer immunotherapy. By genetically engineering patient-derived T cells to express synthetic receptors, CAR-T cells can specifically recognize and eliminate tumor cells. The therapeutic efficacy of CAR-T cells depends heavily on their ability to effectively home to and infiltrate the tumor microenvironment, as well as to specifically recognize tumor-associated antigens on malignant cells.Early studies primarily targeted tumor-associated antigens (TAAs), but these antigens are also expressed in critical normal tissues, and off-tumor toxicity frequently leads to severe adverse events. For example, CAR-T cells targeting carcinoembryonic antigen (CEA) can induce marked but transient colitis, while CAR-T cells targeting MART-1 can damage skin, ocular, or auricular tissues.Researchers subsequently sought tumor-specific antigens (TSAs) as alternative targets; however, naturally occurring TSAs are scarce and difficult to identify. Although CAR-T therapy has achieved striking success in hematologic malignancies, the scarcity of stable antigen targets and the highly immunosuppressive tumor microenvironment have greatly limited its application in solid tumors.Recently, investigators from Shanghai Jiao Tong University in China published an online article in Biomaterials titled "Coated oncolytic viruses based ‘double strike’ strategy triggering CD19 CAR-T therapy in gastrointestinal tumors". To enhance the immunotherapeutic efficacy of CAR-T cells against solid tumors, the team developed an integrated system that employs an oncolytic adenovirus to simultaneously introduce a surface antigen target for CAR-T cells and remodel the immunosuppressive tumor microenvironment. The system uses B cell membrane-derived CD19 as an artificial antigen target displayed on tumor cells and can generate, in situ, an anti-CD3e × anti-epithelial cell adhesion molecule (EpCAM) bispecific T-cell engager, thereby further enhancing the binding and cytotoxicity of CD19 CAR-T cells against tumor cells.Figure 1. A "Double Strike" strategy to trigger CD19 CAR-T thearpy on gastrointestinal tumors was established in this study through a coated oncolytic virus platform. (ZHANG, Haoyu, et al., 2026)Oncolytic viruses offer unique advantages, including selective infection of tumor cells and activation of the tumor immune microenvironment. Through genetic engineering, oncolytic viruses can be armed with cytokines, bispecific T-cell engagers, and immune checkpoint inhibitors to enable multi-component combination therapy. Bispecific T-cell engagers bridge tumor antigens and T-cell receptors and have already achieved clinical success in B-cell malignancies.Cat.No.Product NamePriceOVZ00001RFP Reporter Oncolytic Virus - MeVInquiryOVZ00002SLC5A5 Expressing Oncolytic Virus - MeVInquiryOVZ00003SLC5A5/GFP Expressing Oncolytic Virus - MeVInquiryOVZ00004GFP Reporter Oncolytic Virus - MeVInquiryOVZ00005Luciferase Reporter Oncolytic Virus - MeVInquiryOVZ00006CEA Expressing Oncolytic Virus - MeVInquiryOVZ00007SLC5A5/GFP Expressing Oncolytic Virus - HSV1InquiryOVZ00008Dual Reporter Oncolytic Virus - HSV1InquiryOVZ00009GFP Reporter Oncolytic Virus - HSV1InquiryDespite the promising potential of combining oncolytic viruses with CAR-T therapy, clinical application remains constrained by challenges associated with systemic delivery—notably, pre-existing or rapidly induced anti-viral antibodies—often limiting usage to intratumoral injections. To improve delivery, cell membrane-coating strategies have shown strong potential. Tumor cell membranes possess homotypic targeting capabilities, which can enhance intratumoral delivery, particularly for intravenous administration.In this study, an oncolytic adenovirus expressing αCD3e-αEpCAM (Adv-αCD3e-αEpCAM, Epv) was encapsulated within a fusion membrane derived from B cells and tumor cells, and the fusion membrane was further modified with a glutathione-responsive, disulfide-linked polyethylene glycol long chain (PEG–SS–PEG), resulting in the Epv@CMP delivery system. This design aimed to improve tumor-targeted delivery efficiency and therapeutic outcomes.The αCD3e-αEpCAM bispecific T-cell engager links T cells to tumor cells, while B cell membrane components integrate into the tumor cell surface to provide a CD19 target, together forming a “double strike” strategy that facilitates CD19 CAR-T therapy. The study found that Epv@CMP, when applied to gastrointestinal tumors, further activated the tumor immune microenvironment. Leveraging a three-pronged targeting and activation mechanism, Epv@CMP combined with CD19 CAR-T cells achieved superior therapeutic efficacy.Cat.No.Product NamePriceLVG00001ZscFv(CD19)-CD3zeta?CAR-T?LentivirusInquiryLVG00004ZscFv(CD19)-OX40-CD3zeta?CAR-T?LentivirusInquiryLVG00002ZscFv(CD19)-41BB-CD3zeta?CAR-T?LentivirusInquiryLVG00003ZscFv(CD19)-CD28-CD3zeta?CAR-T?LentivirusInquiryLVG00006ZscFv(CD19)-CD28-OX40-CD3zeta?CAR-T?LentivirusInquiryLVG00005ZscFv(CD19)-CD28-41BB-CD3zeta?CAR-T?LentivirusInquiryAD03313ZHuman?CD19?adenoviral particlesInquiryLV08354Lhuman?CD19?(NM_001770) lentivirus particlesInquiryLV08353Lhuman?CD19?(NM_001178098) lentivirus particlesInquiryLVG00031ZscFv(EGFR)-CD3zeta?CAR-T?LentivirusInquiryLVG00025ZscFv(CEA)-CD3zeta?CAR-T?LentivirusInquiryLVG00037ZscFv(EPCAM)-CD3zeta?CAR-T?LentivirusInquiryLVG00061ZscFv(PSMA)-CD3zeta?CAR-T?LentivirusInquiryLVG00073ZscFv(Control)-CD3zeta?CAR-T?LentivirusInquiryLVG00055ZscFv(MSLN)-CD3zeta?CAR-T?LentivirusInquiryReferenceZHANG, Haoyu, et al. Coated Oncolytic Viruses Based “Double Strike” Strategy Triggering CD19 CAR-T Therapy in Gastrointestinal Tumors. Biomaterials, 2026, 124143.
Myocardial Infarction (MI) leads to the irreversible loss of cardiomyocytes and adverse remodeling, eventually progressing to heart failure (HF). Although gene- and RNA-based therapies offer promising strategies for cardiac repair, current approaches often rely on invasive intramyocardial delivery or are limited by the short duration of expression and low protein yield of traditional mRNA.Consequently, developing a minimally invasive therapeutic platform capable of sustained expression of cardioprotective factors remains a critical unmet need in the field of cardiac therapy.Recently, Professor Ke Cheng's team at Columbia University published a research paper titled "Single intramuscular injection of self-amplifying RNA of Nppa to treat myocardial infarction" in the prestigious international journal Science. The study developed a lipid nanoparticle-delivered self-amplifying RNA therapy (saNppa-LNP). A single intramuscular injection can achieve sustained expression of cardioprotective factors in vivo, significantly improving cardiac function and ventricular remodeling after myocardial infarction, supporting the broader potential of saRNA-LNP-based therapies for treating cardiac diseases.Atrial Natriuretic Peptide (ANP), encoded by the Nppa gene, is a developmentally regulated cardiac hormone with potent cardioprotective functions. The research team previously observed that Nppa expression is induced following myocardial infarction in both neonatal and adult mice; however, the level of induction is significantly higher in the hearts of neonatal mice, which possess strong regenerative capabilities. This disparity suggests that elevated Nppa expression levels may be linked to enhanced cardiac regeneration, whereas the limited repair capacity of adult mouse hearts may be due to insufficient Nppa induction.To address this, the team developed a self-amplifying RNA (saRNA) therapy delivered via lipid nanoparticles (LNPs) to drive additional Nppa expression. Unlike conventional mRNA, saRNA can self-replicate within cells, enabling more persistent protein expression at extremely low doses.Cat.No.Product NamePricePMSAR-0001EGFP saRNAInquiryPMSAR-0002Firefly Luciferase saRNAInquiryPMSAR-0003Nano Luciferase saRNAInquiryPMSAR-0004NLuc-EGFP saRNAInquiryPMSAR-0005Gaussia Luciferase saRNAInquiryPMSAR-0006Renilla Luciferase saRNAInquiryPMSAR-0007mCherry saRNAInquiryPMSAR-0008β-galactosidase saRNAInquiryPMSAR-0009Luciferase P2A GFP saRNAInquiryPMSAR-0010Cas9 saRNAInquiryPMSAR-0011NLS-Cre saRNAInquiryPMSAR-0012Cas9 Nickase saRNAInquiryPMSAR-0013Cas9-T2A-EGFP saRNAInquiryPMSAR-0014Cre-T2A-EGFP saRNAInquiryPMSAR-0015OVA saRNAInquiryThe research team reasoned that a single intramuscular injection of saRNA-LNP encoding native Nppa (saNppa-LNP) could establish an "RNA factory" in the body. This factory continuously produces and secretes Pro-ANP, a precursor that enters the circulatory system. Pro-ANP is then selectively cleaved and activated into functional ANP by Corin—a cardiac protease highly expressed only in the heart. This achieves a "muscle production, cardiac activation" model, providing long-lasting cardioprotection without the need for direct cardiac intervention.Experimental results showed that a single intramuscular injection of saNppa-LNP in mice induced robust Pro-ANP secretion lasting for at least four weeks, outperforming an equivalent dose of mRNA-LNP. In mouse models of acute myocardial infarction and ischemia/reperfusion (I/R) injury, saNppa-LNP treatment significantly increased left ventricular ejection fraction (LVEF), reduced infarct size, and mitigated fibrosis. These therapeutic benefits were consistently validated in aged, atherosclerotic, and diabetic myocardial infarction models. Furthermore, large animal studies in a porcine I/R model confirmed that a single intramuscular injection effectively protected cardiac function and limited adverse cardiomyocyte remodeling.Figure 1. Intramuscular injectable saNppa-LNP therapy for durable cardioprotection. (ZHANG, Kaiyue, et al., 2026)Mechanistically, single-nucleus transcriptomic analysis (snRNA-seq) revealed that saNppa-LNP treatment reshaped the paracrine profiles of natriuretic peptide receptor-1 positive (Npr1+) endothelial and epicardial cells. This created a pro-regenerative microenvironment that promoted cardiomyocyte cell-cycle reentry and inhibited the expansion of pro-fibrotic periostin-positive (Postn+) fibroblasts. Additionally, longitudinal safety assessments showed only transient local inflammation following treatment, with no evidence of adaptive immune activation or systemic toxicity.In conclusion, this study demonstrates that a single intramuscular injection of saNppa-LNP provides robust and lasting cardioprotection across multiple species and clinically relevant injury models. By leveraging the self-amplifying properties of saRNA and the myocardial-specific activation of Pro-ANP, this minimally invasive, single-dose therapy may offer a safe, simple, and effective strategy for cardiac repair.ReferenceZHANG, Kaiyue, et al. Single intramuscular injection of self-amplifying RNA of Nppa to treat myocardial infarction. Science, 2026, 391.6789: edau9394.
Engineered T cells, modified to express Chimeric Antigen Receptors (CAR) or T Cell Receptors (TCR), have revolutionized cancer treatment and are currently being explored for the treatment of autoimmune and infectious diseases. Gene editing to enhance T cell function—whether through the disruption of endogenous genes or the precise insertion of DNA payloads—has demonstrated significant potential.However, the current ex vivo manufacturing process is lengthy and expensive, limiting the accessibility of these therapies. Generating CAR-T cells in vivo could overcome these obstacles, but existing methods rely either on transient expression with limited persistence or on random integration of DNA payloads that lack specificity.Recently, a collaborative study by the teams of Justin Eyquem and Jennifer A. Doudna at the University of California, San Francisco, was published online in Nature, titled "In vivo site-specific engineering to reprogram T cells". This research demonstrates that stable and cell-specific transgene expression can be achieved through site-specific integration of large DNA payloads in vivo. The researchers developed a dual-vector system using an enveloped delivery vehicle (EDV) and an adeno-associated virus (AAV) to deliver the CRISPR-Cas9 nuclease complex and the DNA template, respectively. Both vectors were optimized to achieve specific delivery to T cells and high gene-targeting efficiency.By transducing a CAR gene into a T-cell-specific locus, the study successfully generated therapeutic levels of CAR-T cells in vivo within humanized mouse models of B-cell deficiency, as well as in hematologic and solid tumor models. These findings pave the way for more efficient, precise, and accessible T-cell therapies.CAR-T cells represent a promising approach for treating hematologic malignancies; to date, the U.S. Food and Drug Administration (FDA) has approved seven CAR-T cell therapies. Standard CAR-T therapy requires personalized production for each patient, which is limited by inconsistent product quality, long production cycles, and high costs.Typically, CARs are delivered via retroviral vectors, leading to variability in expression results due to random integration. By using CRISPR-Cas9 and adeno-associated virus (AAV)-mediated homology-directed repair (HDR), the CAR can be targeted for integration into the native human TCRα gene locus (TRAC).TRAC-CAR T cells exhibit dynamic CAR expression, which can delay cell exhaustion and improve tumor control in xenograft and immunocompetent models. This work is crucial for the development of allogeneic CAR-T cell therapies, as it disrupts the TCR upon transgene insertion—a necessary step to limit Graft-versus-Host Disease (GvHD).Clinical trials using allogeneic TRAC-CAR T cells derived from healthy donors or induced pluripotent stem cells (iPSCs), combined with intensive lymphodepletion conditioning, have achieved complete remission in patients with hematologic malignancies. Allogeneic therapies can address manufacturing limitations by creating "off-the-shelf" drugs from healthy donors. However, allogeneic CAR-T cells are eventually rejected by the body, and frequent relapses have been observed.Generating CAR-T cells directly in vivo may bypass the various hurdles encountered during leukapheresis and the manufacturing process. It also has the potential to promote the formation of a less-differentiated CAR-T cell population, a trait associated with enhanced anti-tumor activity.To date, efforts to generate CAR-T cells in vivo have utilized randomly integrating viral vectors for sustained CAR expression or lipid nanoparticles (LNPs) for transient expression. Both methods were recently validated in non-human primates and evaluated in a Phase I clinical trial. These approaches face several challenges, including how to efficiently deliver genes to therapeutic doses while avoiding the risk of off-target transduction.Figure 1. Co-delivery of Cas9-EDV and HDRT-AAV generates TRAC-CAR T cells in vitro and in vivo. (NYBERG, William A., et al., 2026)Both delivery and CAR expression should be T-cell specific, as off-target modification of hematopoietic stem cells (HSCs) could lead to mutagenic transformation. Furthermore, CAR expression in tumor cells could prevent the surface expression of target proteins, leading to antigen-negative relapse. LNP delivery of CAR mRNA results in transient expression, which prevents insertional mutagenesis or stable expression in tumor cells, but the required dosage remains unclear.While the envelopes of lentiviral vectors can be engineered to improve T-cell specificity, any non-T cell that is transduced would also express the CAR—posing a potential risk of insertional mutation unless a cell-lineage-specific promoter is used. The researchers hypothesized that integrating a promoterless CAR transgene into the TRAC locus in vivo would enable T-cell-specific and physiological CAR expression while avoiding the ex vivo manufacturing process. Until now, the precise in vivo integration of large DNA payloads in human T cells had not been achieved.Cat.No.Product NamePriceLVG00031ZscFv(EGFR)-CD3zeta?CAR-T?LentivirusInquiryLVG00055ZscFv(MSLN)-CD3zeta?CAR-T?LentivirusInquiryLVG00025ZscFv(CEA)-CD3zeta?CAR-T?LentivirusInquiryLVG00037ZscFv(EPCAM)-CD3zeta?CAR-T?LentivirusInquiryLVG00061ZscFv(PSMA)-CD3zeta?CAR-T?LentivirusInquiryLVG00073ZscFv(Control)-CD3zeta?CAR-T?LentivirusInquiryLVG00001ZscFv(CD19)-CD3zeta?CAR-T?LentivirusInquiryLVG00007ZscFv(CD20)-CD3zeta?CAR-T?LentivirusInquiryLVG00067ZscFv(TACSTD2)-CD3zeta?CAR-T?LentivirusInquiryLVG00013ZscFv(CD33)-CD3zeta?CAR-T?LentivirusInquiryLVG00019ZscFv(CD38)-CD3zeta?CAR-T?LentivirusInquiryLVG00043ZscFv(GPC3)-CD3zeta?CAR-T?LentivirusInquiryLVG00049ZscFv(HER2)-CD3zeta?CAR-T?LentivirusInquiryLVG00074ZscFv(Control)-41BB-CD3zeta?CAR-T?LentivirusInquiryLVG00039ZscFv(EPCAM)-CD28-CD3zeta?CAR-T?LentivirusInquiryThis study developed a method combining AAV with an enveloped delivery vehicle (EDV) for site-specific transgene integration in primary human T cells in vivo. By optimizing the AAV and EDV tools to improve cell-specific delivery efficiency and enhance resistance to human neutralizing antibodies, the researchers were able to generate therapeutic levels of TRAC-CAR T cells in vivo and control tumor growth in multiple humanized mouse models.ReferenceNYBERG, William A., et al. In vivo site-specific engineering to reprogram T cells. Nature, 2026, 1-10.
Circular RNAs (circRNAs) are primarily generated through the back-splicing of precursor mRNAs, yet their functional targets and underlying mechanisms have remained largely elusive. Recently, researchers from the Institute of Biophysics of the Chinese Academy of Sciences published a research paper titled "Global mapping of circRNA-target RNA interactions reveal P-body-mediated translational repression" online in the journal Molecular Cell. This study introduces circTargetMap—a computational framework for the genome-wide mapping of circRNA targets using RNA-RNA interactomes obtained via RNA in situ conformation sequencing (RIC-seq) across the hippocampus and ten human cell lines. This approach identified 117,163 high-confidence circRNA-target RNA interactions, revealing that 83% of target mRNAs are bound by multiple circRNAs.Functional investigations demonstrated that CDR1as and circRMST sequester target mRNAs into membraneless granules—specifically processing bodies (P-bodies)—through sequence-specific base pairing, thereby inhibiting the translation of these target mRNAs. This process appears to be independent of AGO2, DICER, and microRNAs (miRNAs). To directly capture these granule-associated interactions, the authors developed a method called Granule RIC-seq (GRIC-seq), which revealed a widespread role for circRNA-target RNA interactions in translational repression. Furthermore, pathogenic variants were found to be significantly enriched near circRNA-target RNA interaction sites, suggesting a potential role for these interactions in disease. This research provides a valuable resource for exploring circRNA functions and establishes an analytical framework for studying RNA-RNA interactions within membraneless organelles.CircRNAs are a class of covalently closed RNA molecules formed by the back-splicing of precursor mRNAs. This process connects a downstream splice donor to an upstream splice acceptor site, creating a characteristic back-splice junction (BSJ). This mechanism can generate thousands of distinct circRNAs from various genes. Among them, a subset of circRNAs with high circular-to-linear expression ratios—such as CDR1as (also known as ciRS-7), circRMST, and circHIPK3—exhibit extreme stability and high abundance, and are consistently detected across different cell types and tissues, suggesting evolutionarily conserved regulatory roles. The expression of circRNAs also displays cell-type-specific, tissue-specific, and developmental stage-specific patterns, with particularly high abundance observed in the brain.Cat.No.Product NamePricePMCR-0001EGFP circRNAInquiryPMCR-0002Firefly Luciferase circRNAInquiryPMCR-0003Gaussia Luciferase circRNAInquiryPMCR-0004Renilla Luciferase circRNAInquiryPMCR-0005mCherry circRNAInquiryPMCR-0006β-galactosidase circRNAInquiryPMCR-0007Luciferase P2A GFP circRNAInquiryPMCR-0008Cas9 circRNAInquiryPMCR-0009NLS-Cre circRNAInquiryPMCR-0010Cas9 Nickase circRNAInquiryPMCR-0011Cas9-T2A-EGFP circRNAInquiryPMCR-0012Cre-T2A-EGFP circRNAInquiryPMCR-0013OVA circRNAInquiryPMCR-0014EPO circRNAInquiryPMCR-0015Spike DELTA circRNAInquiryPMCR-0016Spike OMICRON circRNAInquiryPMCR-0017Spike SARS COV-2 circRNAInquiryPMCR-0018HER2/ErbB2 circRNAInquiryAlthough circRNAs have been proven to participate in critical biological processes such as differentiation, cancer, and immune regulation, their target landscapes and mechanisms of action remain unclear. Existing models propose several potential functions for circRNAs, including acting as "molecular sponges" for miRNAs and sequestering RNA-binding proteins (RBPs). The most classic example, CDR1as, contains over 70 conserved binding sites for miR-7, thereby regulating miR-7 availability. Additionally, circRNAs appear to be involved in the regulation of transcription and splicing. However, these functions are primarily derived from isolated case studies, and it remains uncertain whether a broader, generalizable mechanism exists.Given their single-stranded structure and stability, circRNAs may also function through direct base pairing with target RNAs. Recent studies have explored this possibility using 4′-aminomethyl-4,5',8-trimethylpsoralen (AMT)-mediated psoralen crosslinking to capture circRNA-mRNA duplexes, followed by oligonucleotide pull-down and high-throughput RNA sequencing. These methods identified hundreds of circRNAs interacting with mRNAs and several circZNF609-target RNA pairs, but they are limited by low resolution, a lack of precise binding site information, and a reliance on labor-intensive pairwise validation. While bioinformatics predictions for circRNA-mRNA binding sites have been attempted, there is still a lack of a scalable, high-resolution method for the systematic mapping of circRNA-target interactions.Figure 1. Mechanistic Diagram of circTargetMap. (LI, Peng, et al., 2026)This study presents circTargetMap, a computational framework that globally maps circRNA-target RNA interactions by analyzing RIC-seq data—a technology capable of resolving native RNA-RNA interactomes mediated by various RBPs. By applying this framework to data from ten cell lines and human/mouse hippocampi, the authors identified 117,163 high-confidence interactions. They discovered that CDR1as and circRMST inhibit the translation of their targets through direct base pairing—a process independent of Argonaute 2 (AGO2), DICER, or miRNAs—by sequestering targets into membraneless granules such as P-bodies. To map these interactions within granules, the authors developed GRIC-seq, enabling the transcriptome-wide detection of circRNA-mRNA interactions within P-bodies. This revealed a widespread, P-body-mediated mechanism of circRNA-dependent translational repression. Moreover, the significant enrichment of pathogenic variants around circRNA-target RNA junction regions suggests that the disruption of these RNA-RNA interactions may be linked to disease.ReferenceLI, Peng, et al. Global mapping of circRNA-target RNA interactions reveal P-body-mediated translational repression. Molecular Cell, 2026, 86.5: 868-884. e13.
Chimeric Antigen Receptor (CAR)-Natural Killer (NK) cell therapy holds great promise for treating solid tumors. Still, its application remains limited due to poor infiltration, persistence, and resistance of CAR-NK cells within the tumor microenvironment (TME).Recently, Sidi Chen and Lei Peng from Yale University published a research paper in Nature titled "OR7A10 GPCR engineering boosts CAR-NK therapy against solid tumours". To identify synergistic targets capable of enhancing CAR-NK cell efficacy, the study conducted an unbiased in vivo CRISPR activation (CRISPRa) screen, followed by a barcoded targeted in vivo open reading frame (ORF) screen in primary human CAR-NK cells. The study identified and comprehensively validated OR7A10, a G protein-coupled receptor (GPCR), as the optimal candidate.Figure 1. In in vivo CRISPRa and barcoded ORF screening experiments, OR7A10 was identified as a key factor in enhancing the anti-tumor efficacy of CAR-NK cells. (YANG, Luojia, et al., 2026)By engineering CAR-NK cells to encode OR7A10 cDNA—a method that bypasses CRISPR technology and utilizes a simple manufacturing strategy—the researchers enhanced their proliferation, activation, degranulation, cytokine production, death ligand expression, chemokine receptor expression, cytotoxicity, persistence, metabolic fitness, and resistance to the tumor microenvironment.Cat.No.Product NamePriceAD11576ZHuman OR7A10 adenoviral particlesInquiryLV20634Lhuman OR7A10 (NM_001005190) lentivirus particlesInquiryCDFH013441Human OR7A10 cDNA Clone(NM_001005190.1)InquiryMiUTR1H-07350OR7A10 miRNA 3'UTR cloneInquiryFurthermore, exhaustion was mitigated in primary human NK cells derived from multiple peripheral blood and umbilical cord blood donors. OR7A10-enhanced CAR-NK cells demonstrated robust in vivo efficacy across various solid tumor models. For instance, in an orthotopic breast cancer mouse model, a 100% complete response was achieved, along with long-term tumor control and survival benefits. These findings suggest that OR7A10-engineered CAR-NK cells can serve as a highly effective and mass-producible off-the-shelf therapy for solid tumors.NK cells are cytotoxic lymphocytes with powerful capabilities for anti-tumor activity and the clearance of virus-infected cells. They can bypass Major Histocompatibility Complex (MHC) restrictions and prior immune stimulation. By recognizing gene-encoded ligands associated with oncogenic transformation, NK cells can target cancer cells with low mutational burdens or those lacking neoantigen presentation.Adoptive CAR-NK cell therapy is relatively safe, carries almost no risk of Graft-Versus-Host Disease (GVHD) or Cytokine Release Syndrome (CRS), and is suitable for large-scale industrial production. These advantages have driven research into developing NK-cell-based therapies for solid tumors. As of 2025, over 1,200 clinical trials are evaluating NK cells, including more than 160 trials for CAR-NK cell therapies (ClinicalTrials.gov). In fact, trials have already demonstrated favorable results in treating hematological malignancies.While CAR-NK cell therapy has immense potential for solid tumors, key challenges remain, including limited tumor infiltration, insufficient proliferation, and poor persistence within the tumor microenvironment (TME). Currently, various strategies are being investigated to overcome these limitations, including cytokine engineering and the knockout of inhibitory regulators such as CISH, NKG2A, HIF1A, CALHM2, or CREM33.Although gene knockouts can enhance NK cell function, this approach relies on CRISPR-mediated gene editing, which increases the complexity of cell therapy manufacturing. An alternative strategy involves incorporating "enhancers"—genes with the function of driving overexpression—into the CAR construct, providing a simple and scalable solution for CAR-NK cell manufacturing.This study performed in vivo CRISPRa screening on primary human CAR-NK cells, followed by a targeted small-scale screening of in vivo labeled ORFs, to identify genes that enhance anti-tumor activity in vivo upon overexpression (referred to as "super-enhancers" or "enhancers"). Through these experiments, the study identified a highly potent gene, OR7A10, which boosts CAR-NK cell function and demonstrates powerful anti-tumor effects in vivo.ReferenceYANG, Luojia, et al. OR7A10 GPCR engineering boosts CAR-NK therapy against solid tumours. Nature, 2026, 1-12.
Integrating artificial intelligence (AI) with advanced robotics to create self-driving labs (SDLs) is a promising approach to solving challenges in molecular discovery. A new SDL system named LUMI-lab combines large-scale molecular pre-training, active learning, and robotics to discover that brominated lipids—previously unrelated to mRNA delivery—can enhance the efficiency of mRNA entry into human cells. This study, led by researchers at the University of Toronto’s Leslie Dan Faculty of Pharmacy, was published in the journal Cell.Supported by an AC Translational Research Grant from the University of Toronto’s Acceleration Consortium, LUMI-lab integrates a molecular foundation model with an automated robotic system. To the research team’s surprise, it identified a new class of mRNA-enhancing lipids—brominated lipid tails—as primary enhancers for increasing transfection efficiency.“Through ten active learning cycles, LUMI-lab synthesized and tested over 1,700 novel lipid nanoparticles (LNPs), discovering brominated ionizable lipids that deliver mRNA into human lung cells with higher efficiency than approved benchmarks,” said Bowen Li, the GSK Chair in Pharmaceutics and Drug Delivery at the University of Toronto’s Leslie Dan Faculty of Pharmacy and an affiliate scientist at the Princess Margaret Cancer Centre, University Health Network. “The key advancement of this AI-driven system is that it independently identified bromination as a significant and meaningful feature without a prior hypothesis and without researchers telling it to look for it first.”Cat.No.Product NamePricePMmRNL-0001EGFP mRNA-LNPInquiryPMmRNL-0002mCherry mRNA-LNPInquiryPMmRNL-0003Firefly Luciferase mRNA-LNPInquiryPMmRNL-0004Cas9-HA mRNA-LNPInquiryPMmRNL-0005EGFP mRNA (no modificaiton)-LNPInquiryPMmRNL-0006mCherry mRNA (no modificaiton)-LNPInquiryPMmRNL-0007Firefly Luciferase mRNA (no modificaiton)-LNPInquiryPMmRNL-0008spCas9 mRNA (no modificaiton)-LNPInquiryPMmRNL-0009spCas9 mRNA (N1-Me-Pseudo UTP modified)-LNPInquiryPMmRNL-0010SARS COV-2 Spike Protein (Alpha Variant) mRNA-LNPInquiryWhile mRNA therapies are one of the fastest-growing drug modalities, they currently rely on lipid nanoparticles for safe delivery to target areas in the human body. To date, only three LNPs have received FDA approval. Platforms like LUMI-lab are expanding the design space by accelerating the discovery of next-generation LNPs needed to unlock new therapeutic applications.Furthermore, SDL models for drug discovery typically rely on large, high-quality datasets to perform well. In emerging fields like mRNA therapy development and delivery, the scarcity of historical data remains a major obstacle. To address this data shortage, the team opted for a foundation-based model, pre-training LUMI-lab on over 28 million molecular structures to allow it to learn general chemical patterns and structures before undertaking more specific tasks.Figure 1. LUMI-lab is a powerful, data-efficient platform for autonomous discovery and optimization of molecules. (Xu, Y., et al., 2026)“When integrated into an active learning framework, the model can be continuously optimized in a closed-loop workflow, further improving its predictive accuracy,” said Li, who also serves as the Canada Research Chair in RNA Vaccines and Therapeutics.When tested in preclinical models, several newly discovered lipids outperformed the lipids used in Moderna’s COVID-19 mRNA vaccine. Although brominated lipids accounted for only 8% of the compound library used by LUMI-lab, they represented more than half of the top-performing candidates. Brominated lipids also demonstrated a safety profile similar to clinical benchmarks, supporting their potential for future therapeutic development.“Next, we are expanding LUMI-lab to simultaneously optimize multiple clinically relevant attributes—not just delivery potency, but also safety, tolerability, and tissue selectivity,” Li said. “Through closed-loop AI predictions and automated experimentation, our goal is to shorten the design cycles for novel lipid materials and open up a larger, evidence-driven chemical space for mRNA therapies.”ReferenceXu, Y., et al. LUMI-lab: A foundation model-driven autonomous platform enabling discovery of ionizable lipid designs for mRNA delivery. Cell, 2026.
