About

Corinne Beinat is an Assistant Professor of Radiology at Stanford University, specializing in Molecular Imaging. She holds a PhD in Medicinal Chemistry from The University of Sydney, obtained in 2014, and a BSc (Hons) in Organic Chemistry and Pharmacology from The University of Sydney, earned in 2009. Her academic background and research focus are centered on advancing molecular imaging techniques within the field of radiology, contributing to the development of innovative diagnostic and therapeutic approaches.

Research topics

• Immunology
• Cancer research
• Biology
• Computer Science
• Physics
• Biochemistry
• Pathology
• Internal medicine
• Acoustics
• Medicine
• Materials science
• Nanotechnology
• Chemistry
• Telecommunications
• Virology

Selected publications

• MUC1-targeting small peptide radiopharmaceuticals for breast cancer

  EJNMMI Radiopharmacy and Chemistry · 2026-05-02

  articleOpen accessSenior author

  BACKGROUND: Mucin 1 (MUC1) is a transmembrane glycoprotein overexpressed and underglycosylated in numerous epithelial cancers, including breast cancer. Reduced glycosylation leads to the exposure of the variable number tandem repeat (VNTR) region. To the best of our knowledge, all peptides previously described in the literature target the same epitope sequence of the VNTR. Given the high prevalence of breast cancer and the limited treatment options for the aggressive subtype triple-negative breast cancer (TNBC), due to its lack of oestrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2), we sought to develop a small peptide radiopharmaceutical targeting MUC1 by exploring all 3 minimal epitope sequences of the VNTR: RPAPGS, PPAHGVT and PDTRP. We also investigated the influence of linker lipophilicity on the binding affinity to MUC1. RESULTS: Lu]-labelled peptides tested. Given the discrepancies between our cell data and the previously reported results, we next assessed the specificity of the reference (1) in vivo in mice bearing MUC1-expressing and MUC1-knockdown (KD) tumours, which further proved its non-specificity. CONCLUSIONS: While MUC1 is a very promising target for the development of breast cancer theranostics, designing peptidomimetics based on its minimal epitopes do not lead to high-affinity binders. Our ongoing efforts involve utilizing phage-display to identify new peptide sequences.

  PublisherDOI

• [18F]DASA-23 PET/MRI evaluation in newly-diagnosed and recurrent high-grade glioma

  Neuroradiology · 2026-04-01

  articleOpen access

  High-grade gliomas pose significant diagnostic imaging challenges in their initial diagnosis, evaluation of treatment-related change versus recurrent/progressive disease, and prognostication. 1-((2-fluoro-6-[18F]fluorophenyl)sulfonyl)-4-((4-methoxyphenyl)sulfonyl)piperazine ([18F]DASA-23) which binds pyruvate kinase M2 (PKM2), an important enzyme in glycolysis, was developed to probe the metabolic activity of high-grade gliomas. This pilot study sought to evaluate [18F]DASA-23 PET’s diagnostic performance in high-grade gliomas, how its uptake over time is associated with survival, and its relationship with conventional MR findings. This prospective pilot study enrolled healthy controls and patients with high-grade gliomas who received [18F]DASA-23 PET/MRI’s. In the latter group, scans were performed at the time of initial diagnosis or recurrence, with a sub-group also receiving follow-up scans during their therapy course. Three nuclear medicine physicians independently adjudicated the presence or absence of focal intracranial [18F]DASA-23 uptake, from which the sensitivity, specificity, accuracy, positive predictive value, and negative predictive value were determined. For patients with tumors, tumor-to-background SUVmax was calculated and correlated with progression-free survival (PFS). Correlation analysis between MRI perfusion parameters and [18F]DASA-23 TBRmax was also performed. As an exploratory analysis, the amount of [18F]DASA-23 uptake overlap with sites of both MRI T1 post-contrast enhancement and non-enhancing T2-FLAIR hyperintense signal about the resection cavity pre-therapy was determined. Four healthy controls and nine patients with high-grade gliomas were included in this study. The baseline [18F]DASA-23 PET demonstrated a sensitivity of 0.78, specificity of 1.00, and accuracy of 0.85 in the diagnosis of high-grade glioma. The follow-up [18F]DASA-23 PET exams in 5 patients at a mean of 46 days after initiation of therapy showed tumor to background ratio SUVmax (TBRmax) was significantly inversely correlated with PFS (r = -0.91, p = 0.03). MR dynamic contrast susceptibility (DSC) derived normalized cerebral blood volume (nCBV) and arterial spin labeling (ASL) derived normalized cerebral blood flow max (nCBFmax) were not significantly associated with [18F]DASA-23 uptake. Within the [18F]DASA-23 uptake regions of interest, 20.2% of the volume was occupied by T1 post-contrast enhancement, and 28.3% of the volume was non-enhancing T2 FLAIR hyperintensity, with no significant difference in the volume of enhancement and non-enhancing T2 FLAIR hyperintensity. This pilot study demonstrated favorable [18F]DASA-23 PET diagnostic performance in the diagnosis of high-grade gliomas, and its uptake after initiation of therapy may with further research be useful as a marker to evaluate treatment efficacy and patient prognosis. Additionally, the absence of a significant relationship between [18F]DASA-23 uptake and MR perfusion markers, and [18F]DASA-23 PET’s limited overlap with enhancement and non-enhancing T2 FLAIR hyperintensity raises the possibility that future [18F]DASA-23 PET studies with larger patient samples could uncover clinically relevant information not fully captured with MR alone.

  PublisherOA PDFDOI

• A Novel Murine Model to Study the Early Biological Events of Corticosteroid-Associated Osteonecrosis of the Femoral Head

  Bioengineering · 2026-01-20

  articleOpen access

  F-fluorodeoxyglucose positron emission tomography/computed tomography (PET/CT) and changes in key histologic markers of bone over a 6-week period. Sixteen 12-week-old Balb/C mice were divided into two groups: a prednisolone group (PRED) and a control group (SHAM). The PRED group received a subcutaneous 60-day sustained-release pellet containing 2.5 mg of prednisolone, while the SHAM group received placebo pellets. PET/CT imaging was performed at 1, 3, and 6 weeks. Bone mineral density (BMD) measurements, and histomorphological analyses for the number of empty lacunae, osteoblasts, osteoclasts, and NADPH oxidase (NOX) 2, a marker for oxidative stress, were conducted at 4 or 6 weeks. PET/CT imaging demonstrated increased uptake in the femoral head at 3 weeks in the PRED group. This was accompanied by increased numbers of empty lacunae and osteoclasts, increased oxidative stress, and decreased alkaline phosphatase staining at 4 weeks in the PRED group. We have successfully established and validated a small murine model of ONFH. The findings of this preclinical study suggest a critical timeline for potential interventions to mitigate the early adverse effects of continuous corticosteroid exposure on bone.

  PublisherOA PDFDOI

• A radiolabeled dendrimer non-invasively identifies and tracks innate immune cell activation in a mouse model of experimental autoimmune encephalomyelitis

  Nature Communications · 2026-01-30

  articleOpen access

  Multiple sclerosis (MS) is a chronic neurodegenerative disease driven by infiltration of activated innate immune cells into the central nervous system (CNS). Current imaging approaches for diagnosing and monitoring disease progression rely on structural lesions and cannot directly assess innate immune activity. Here, we describe a dendrimer positron emission tomography (PET) tracer, 18F-flurimedrimer (18F-FMD), for non-invasive, longitudinal tracking of activated myeloid cells. In an experimental autoimmune encephalomyelitis (EAE) murine model, 18F-FMD specifically detects myeloid activation at presymptomatic and symptomatic stages, with PET signal correlating with disease severity. Moreover, 18F-FMD sensitively captures therapeutic response to fingolimod (FTY720) and a CSF1R dendranib (H74DS3M8), both of which suppress immune cell activation and attenuate disease severity. These findings highlight the potential of 18F-FMD PET for specific, real-time monitoring of innate immune responses, and the applicability of the dendrimer in clinical settings for monitoring therapeutic efficacy, advancing the development of personalized, myeloid-targeted strategies for MS. Non-invasive strategies to detect and track activated myeloid cells will facilitate disease diagnosis and monitoring in patients affected by neuroinflammatory disorders. Here, the authors present 18F-FMD, a dendrimer-based PET tracer that detects and monitors activated myeloid cells at different stages (presymptomatic and symptomatic) of Experimental Autoimmune Encephalomyelitis (EAE) in mice and in response to disease-modifying therapies.

  PublisherDOI

• Ultrasound-Mediated Gene Therapy in Alzheimer’s Disease Validated through In Vivo PET Imaging

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-04

  articleOpen access

  Efficient, spatially selective delivery of adeno-associated virus (AAV) therapeutics to deep brain structures remains a major challenge to gene therapy for Alzheimer's disease (AD), owing to limited transport across the blood-brain barrier (BBB) and poor penetration to target neurons. Here, we establish an integrated, noninvasive imaging and therapy platform that combines microbubble-enhanced focused ultrasound (MB-FUS) with positron emission tomography/computed tomography (PET/CT) to transiently modulate the BBB, enhance region-specific AAV delivery following systemic dosing, and longitudinally track transduction in vivo. Optimized MB-FUS achieved targeted hippocampal delivery of systemically administered AAV9 in healthy mice, resulting in a 10-fold enhancement of neuronal transduction as compared to non-FUS controls. Importantly, longitudinal PET reporter gene imaging in the 5xFAD AD model demonstrated robust brain AAV transduction that remained stable for at least seven months. Finally, to assess therapeutic impact, we used brain-derived neurotrophic factor (BDNF) as a test cargo. MB-FUS-facilitated delivery elevated BDNF expression in targeted regions and produced short-term improvements in synaptic signaling in 5xFAD mice. Collectively, these results highlight MB-FUS as a next-generation delivery platform to overcome barriers to AAV therapeutic delivery in Alzheimer's disease and position longitudinal PET assessment as a critical, translatable tool for monitoring and optimizing gene therapy.

  PublisherOA PDFDOI

• Illuminating proinflammatory myeloid cells with PET tracers targeting GPR84

  Proceedings of the National Academy of Sciences · 2026-05-21

  articleOpen access

  Innate immunity mediated by myeloid cells defends against infection and injury, but when chronically activated, it drives tissue damage and neurodegeneration. Molecular imaging with positron emission tomography (PET) enables noninvasive, real-time monitoring of such processes in vivo. However, most current neuroinflammation PET tracers lack specificity for activated myeloid cells. G protein–coupled receptor 84 (GPR84) is a promising biomarker that is selectively upregulated on activated microglia and macrophages. Here, we report the development and validation of two fluorine-18-labeled GPR84 tracers, [ 18 F]MGX-110S and [ 18 F]MGX-111S. Both exhibit specific binding to human GPR84-expressing cells, with [ 18 F]MGX-110S demonstrating superior affinity, selectivity, and signal-to-background ratio. [ 18 F]MGX-110S enables sensitive detection of systemic- and neuro-inflammation in LPS-treated mice and outperforms PET images obtained using a radiotracer specific for translocator protein 18 kDa in 5xFAD mice—revealing pathology-correlated activation across cortical, hippocampal, and thalamic regions. Taken together, our data indicate that [ 18 F]MGX-110S is a highly sensitive and specific tool for visualizing maladaptive myeloid cell activation; its clinical translation could enable more precise detection and staging of inflammation in addition to improved therapeutic monitoring in neurodegenerative disorders and more broadly in inflammatory diseases.

  PublisherOA PDFDOI

• Augmentation of [18F]-C-SNAT4 PET imaging of apoptosis after radiotherapy using a cold mixing strategy

  EJNMMI Research · 2025-06-03

  articleOpen access

  BACKGROUND: Positron Emission Tomography (PET) imaging can monitor cancer treatment response by non-invasively detecting apoptosis in vivo. Signal-to-noise (SNR) remains one of the critical barriers to approval for clinical use. We have previously developed a PET tracer [18 F]-C-SNAT4 for imaging capase-3 activity in apoptotic tumors induced by chemo- and immunotherapy. [18 F]-C-SNAT4 is designed to undergo caspase-3 activated intramolecular cyclization. The product then self-assembles in situ into nanoparticles to generate preferential retention of F18 radioactivity in apoptotic cells. This unique mechanism prompted us to investigate if a cold mixture could enhance the probe retention and further augment the sensitivity for imaging radiotherapy. RESULTS: [18 F]-C-SNAT4 and hot/cold mixture [18 F]/[19 F]-C-SNAT4 were used to detect human NSCLC (NCI-H460) apoptosis induced by radiation. Both hot [18 F]-C-SNAT4 and hot/cold mixture [18 F]/[19 F]-C-SNAT4 had significantly increased uptake in radiation treated vs. untreated NCI-H460 cells in vitro. A 1: 80 hot/cold mixture increased signal by 1.6x compared to [18 F]-C-SNAT4 alone. In vivo studies were performed in murine xenograft models in high-dose radiation and low-dose radiation treatment groups. The hot/cold mixture showed an increase in the signal by 2.5x in high-dose radiation treated murine NCI-H460 xenograft models. Low-dose radiation induced apoptosis was only detected with the hot/cold mixture with 2.4x signal compared to hot [18 F]-C-SNAT4. Toxicity and dosimetry safety were evaluated at 250x and 10x respective dosages, then normalized to human dose equivalent. CONCLUSION: A hot/cold mixture of [18 F]/[19 F]-C-SNAT4 generates significantly more signal compared to hot [18 F]-C-SNAT4, leading to higher sensitivity in detecting treatment response. This may present a solution to low sensitivity in the translation of apoptosis-specific radionuclides to clinical application.

  PublisherOA PDFDOI

• Cholesterol in mRNA‐Lipid Nanoparticles can be Replaced with the Synthetic Mycobacterial Monomycoloyl Glycerol Analogue MMG‐1

  Advanced Functional Materials · 2025-08-15 · 3 citations

  articleOpen access

  Abstract Messenger RNA (mRNA) vaccines based on lipid nanoparticles (LNPs) are stabilized with cholesterol, which is thought to be a critical LNP component because it is essential for membrane integrity and endosomal escape. Here, it is shown that cholesterol in LNPs can be replaced with an immunopotentiating lipid, i.e., a synthetic analogue of the C‐type lectin receptor agonist monomycoloyl glycerol (MMG‐1), without compromising physicochemical properties, in vivo transfection efficiency, and immunogenicity of the mRNA‐loaded LNPs (mRNA‐LNPs). Replacement of cholesterol with MMG‐1 results in LNPs that mediate intracellular delivery of mRNA, which is translated into high levels of protein in vivo. Replacement of cholesterol with MMG‐1 in LNPs improves the transfection efficiency in T cells, B cells, and macrophages in the spleen and lymph nodes of mice. In mice, MMG‐1‐based LNPs loaded with mRNA encoding the spike (S) protein of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) induce S‐specific CD8 + T‐cell responses and virus‐neutralizing antibody responses, which are on par with the responses induced by cholesterol‐based LNPs. Upon vaccination and a subsequent SARS‐CoV‐2 challenge of Syrian golden hamsters, replacement of cholesterol with MMG‐1 in mRNA‐LNPs enhances S‐specific immunoglobulin G titers and reduces the SARS‐CoV‐2 load in the nasal cavity. These findings provide insights for improved design of LNPs for mRNA vaccine delivery.

  PublisherOA PDFDOI

• Radiolabeled dendrimer non-invasively tracks innate immune activation in multiple sclerosis mice after immunomodulatory therapy

  Research Square · 2025-02-05

  preprintOpen access
  PublisherOA PDFDOI

• TMET-23. 2-Methylglutamate Prolongs Survival in a Mouse Model of Glioblastoma

  Neuro-Oncology · 2025-11-01

  articleOpen accessSenior author

  Abstract Glutamate plays a central role in glioblastoma (GBM) pathophysiology, promoting tumor proliferation, excitotoxicity, and immune suppression. Emerging evidence also highlights that glioma cells integrate into normal neural circuits, and this neuronal activity drives GBM growth and progression through formation of direct glutamatergic synapses between neurons and glioma cells. Recent work by Wawro et al. (Sci Rep, 2021) demonstrated that enantiomers of 2-methylglutamate (2MeGlu), a glutamate analog, differentially modulate brain metabolism and behavior through stereoselective interactions with glutamate transport and glutamine metabolism. However, the impact of 2MeGlu on glioblastoma progression has not been studied. We employed two orthotopic mouse models of human GBM using luciferase-labeled U251 and GBM39 patient-derived xenograft cells. Approximately nine days post-implantation, mice received daily intraperitoneal injections of a racemic mixture of 2MeGlu (500 mg/kg) or vehicle control. Survival was monitored as the primary endpoint. The control and treatment groups were followed until humane endpoints were met. Tumor burden was assessed weekly using bioluminescence imaging (BLI). U251 glioma-bearing mice exhibited median survival of 26 and 35 days in the control and treatment groups, respectively (p = 0.0165). In GBM39 orthotopic xenografts, median survival of controls was 32 days. In contrast, mice treated with racemic 2MeGlu exhibited median survival of 51 days (p = 0.0004), representing a 59% increase in overall survival compared to controls. Longitudinal BLI revealed lower tumor-associated luminescence in treated animals relative to controls, consistent with reduced intracranial tumor burden. The substantial survival benefit suggests 2MeGlu may modulate glutamate-dependent metabolic or signaling pathways critical to glioblastoma growth or microenvironmental adaptation. These findings provide the first evidence that 2MeGlu confers a survival benefit in a preclinical GBM model. Given prior evidence of stereospecific effects of 2MeGlu on glutamate-glutamine cycling, future work will assess individual enantiomers for differential therapeutic efficacy and potential mechanisms of action, including altered tumor metabolism, immune microenvironment modulation, or excitotoxic stress. These studies may help establish new therapeutic vulnerabilities in glutamate-dependent glioblastoma progression.

  PublisherOA PDFDOI

Frequent coauthors

• Sanjiv S. Gambhir

  Stanford University

  65 shared

• Surya Murty

  47 shared

• Israt S. Alam

  46 shared

• Tom Haywood

  46 shared

• Chirag B. Patel

  The University of Texas MD Anderson Cancer Center

  45 shared

• Lawrence D. Recht

  Stanford Medicine

  30 shared

• Michelle L. James

  Stanford University

  28 shared

• Lewis Naya

  Stanford Cancer Institute

  27 shared

Labs

• Vice Provost for Student AffairsPI

Education

• Postdoctoral Fellow, Radiology

  Stanford Medicine

  2019

• PhD, Chemistry

  The University of Sydney

  2014

• Bachelor of Science (Honours)

  The University of Sydney

  2009