Biology subjects

Prasad, S.

Publications and source records attributed to Prasad, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Involvement of Mitophagy in Endothelin-1 Mediated Neurodegeneration in Rodent Models of Glaucoma

The ultimate cause of blindness in glaucoma is the death of retinal ganglion cells, and understanding the mechanism behind retinal ganglion cell loss during glaucoma could lead to the development of novel treatments for glaucoma. Endothelin-1 has been shown to mediate retinal ganglion cell death during glaucoma through impairment of mitochondrial function. Retinal ganglion cells are highly metabolically active, and susceptible to oxidative damage and decreased respiratory capacity. Mitophagy is the process whereby damaged mitochondria are degraded to prevent further propagation of oxidative damage. The current study evaluates the effect of endothelin-1 on mitophagy in retinal ganglion cells. Electron microscopy revealed endothelin-1 administration lead to a decrease in healthy mitochondria in the optic nerve. The MitoQC mouse was used to evalute mitophagy in response to endothelin-1, along with immunohistochemical analysis of mitophagy proteins. Mitophagy follows different trends in the optic nerve and retinal ganglion cell bodies following endothelin-1 administration, mitophagy was increased in the optic nerve but decreased in the retina following endothelin administration. With elevation of intraocular pressure, mitophagy was increased in the retina but decreased in the optic nerve. In retinal ganglion cells, parkin expression and activation was unchanged 24 hours after endothelin-1 administration, but was decreased 72 hours following endothelin-1 administration. Taken together, these results suggest that endothelin-1 impacts mitophagy through parkin-independent mechanisms in retinal ganglion cell bodies, and the ganglion cell bodies and optic nerve appear to have different responses to endothelin-1.

neuroscience↗

bioRxiv2026

Modular Assembly of an Infectious Clone of the Akata strain of EBV using Synthetic Genomics Methods in Yeast

We have used synthetic biology recombination methods in yeast to build herpes simplex virus type-1 (HSV-1) and human cytomegalovirus (HCMV) genomes from multiple fragments. The genomes were built using transformation-associated recombination (TAR) in yeast, by virtue of overlapping sequences between the different fragments. This study demonstrates the successful assembly of the Epstein-Barr virus (EBV) genome. We used as the model genome, the Akata Burkitts lymphoma genome, specifically the BX1 genome which encodes a neomycin selectable marker and a GFP expression cassette in the BXLF1 region. The 171.3 kb genome was first deconstructed into 11 fragments in silico, each having 80 bp overlapping sequence between the fragments. The 11 fragments (TAR 1 to TAR 11) were cloned using TAR in yeast, analyzed by restriction enzyme analyses and Nanopore sequencing to validate the cloned fragment. The EBV genome was built in two stages: TAR fragments 1 to 6 and TAR fragments 7 to 11 were assembled to generate two half-genomes. The whole genome (TAR 1-11) was then assembled by joining TAR 1-6 with TAR 7-11. Complete EBV genomes were examined by PCR assays and restriction enzyme analyses and then transfected into HEK-293 cells to generate virus producer cell lines. The HEK-293 cell clones were tested for virus production following lytic induction using baculovirus transduction of Zta, Rta and glycoprotein B (BALF4). The supernatants from these induced cells were harvested and used to infect Raji cells. This analysis revealed a significant number of cells displaying strong GFP fluorescence indicative of infectious virus. We used this supernatant virus to infect primary B cells and were able to derive lymphoblastoid cell lines (LCL) indicative of the ability of this virus to transform B cells. We tested this method for engineering different mutations. Two mutations were made, one in Zta and the other in the small capsid protein (BFRF3). Mutations were engineered in the TAR plasmid in which the genes reside and after sequence validation, assembled into the TAR 1-6 half genome and then the TAR 1-11 genome, which was used to generate HEK-293 cell clones. For the {Delta}Zta cell lines, we could detect virus in the supernatants only if baculovirus expressing Zta in trans was included, this {Delta}Zta EBV virus could transform B cells. The small capsid protein (BFRF3) decorates the capsid shell and is required for capsid assembly in a self-assembly system. When the HEK-293 cell clones were induced using co-expression of Zta, Rta and gB, no virus was detected in the culture supernatants. However, if we provided BFRF3 in trans using baculovirus expressing this protein, virus was detected in the supernatants. This provides the first report of the essential role of the small capsid protein in EBV-infected cells.

Synthetic Biology↗

bioRxiv2026

Multimodal Hypersampling of the adult human heart resolves tissue-specific cell states and disease-associated variants

Cardiovascular diseases often arise in anatomically specialised regions of the heart that remain poorly represented in existing single-cell and spatial atlas references. Here we profiled 28 regions of the adult human heart from 36 donors, combining paired single-nucleus RNA and chromatin accessibility assays with spatial transcriptomics. The resulting atlas integrates 1,059,175 expression profiles and 452,614 chromatin accessibility profiles, and defines spatial niches across the heart. In cardiac valves, we identify a valve fibroblast-macrophage niche that is polarised to the non-fibrosa surface and expands with age. Aortic stenosis genetic risk was enriched in inflammatory regulatory programmes of the Valve Fibroblast Immune cell state. In pulmonary veins, we define PITX2+ Myocardial Sleeve Cells, a region-restricted cardiomyocyte population in which a fine-mapped 4q25 atrial fibrillation variant intersects a cell type-specific open chromatin region. In coronary arteries, we resolve a RUNX1-marked synthetic smooth muscle layer in the subintima that provides a molecular identity for diffuse intimal thickening, a constitutive feature of the healthy vessel wall and a substrate for atherosclerosis, and show by perturbation in human smooth muscle cells that RUNX1 promotes cell-cycle entry while restraining inflammatory cytokine gene expression. Finally, allele-specific accessibility together with deep learning models fine-tuned to predict regulatory activity from DNA sequence identify cell type-specific regulatory effects at GWAS loci for atrial fibrillation, coronary artery disease and calcific aortic valve stenosis, including a variant whose Valve Fibroblast-specific effect on the polyamine transporter ATP13A3 is opposite in direction to the effect seen in bulk-tissue eQTL references that lack valve cells. Together with these cardiac sequence models and CardioSleuth, an AI-powered exploration engine for cardiac regulatory effects, this atlas links cardiac anatomy, gene regulation and disease genetics at single-cell resolution. By placing genetic risk in its precise cellular and anatomical context, it provides a foundation for mechanistic disease understanding, cell-state-specific therapeutic target nomination, and improved interpretation of inherited cardiovascular risk to inform future therapy and management.

Cell Biology↗

bioRxiv2026

Nipoppy: A framework for standardizing neuroimaging studies to facilitate international derived-data sharing

Neuroimaging data management and processing are tedious and error-prone, prompting reproducibility concerns. Globally, studies with heterogeneous infrastructure and governance policies lead to eclectic data processing and sharing, necessitating standardization of data workflows to ensure reusability and comparability of multi-centric datasets. The Nipoppy neuroinformatics framework facilitates such standardization by combining specification, protocol, and software to manage study-level data workflows. With its adoption, researchers can share standardized, derived datasets enabling efficient, reproducible, and inclusive research.

bioinformatics↗

bioRxiv2026

Probing voltage dependence interaction of cationic peptides with bacterial porins at a single-molecule level

This study investigates the interaction between the cationic antimicrobial peptide protamine and bacterial porin OmpF (E. coli) at the single-molecule level. Using high-resolution conductance measurements in planar lipid bilayers, strong voltage- and concentration-dependent ion current blockages with OmpF, indicating significant protamine binding were observed. Further analysis revealed that peptide length influences binding kinetics, with longer peptides showing reduced affinity and slower exchange rates. These findings demonstrate that OmpF is a tractable model for studying cationic peptide-channel interactions and translocation mechanisms relevant to antimicrobial action.

biophysics↗

bioRxiv2026

Reduced Prefrontal PRDM2 Increases Stress-Induced Reinstatement Across Sexes via a dmPFC-Nucleus Accumbens Pathway

Stress is a major driver of relapse in alcohol use disorder (AUD), partly through stress-induced dysregulation of prefrontal cortex (PFC) circuits that govern executive control, craving regulation, and adaptive behavioral responses. Such dysfunction may be partly driven by epigenetic regulation of transcriptional programs that shape PFC responses to stress. Here, we investigated the role of the histone methyltransferase PRDM2 in stress-induced relapse to alcohol seeking. Analysis of postmortem human tissue showed that PRDM2 expression in the PFC was reduced in both men and women with AUD compared with control individuals. To examine the functional significance of this reduction in alcohol-related behaviors, we used viral-mediated knockdown of Prdm2 in the dorsomedial prefrontal cortex (dmPFC) of male and female rats. Prdm2 knockdown increased vulnerability to stress-induced reinstatement of alcohol seeking in both sexes, without altering pain sensitivity or being influenced by estrous cycle stage. To determine whether this effect was mediated through specific prefrontal output pathways, we selectively reduced Prdm2 expression in dmPFC neurons projecting to the nucleus accumbens (NAc). Projection-specific knockdown also increased stress-induced reinstatement of alcohol seeking in male and female rats in a shock intensity-dependent manner. Together, these findings suggest that reduced PRDM2 expression in the PFC contribute to stress-induced relapse-like behavior and identify the dmPFC-NAc projection as a circuit through which PRDM2 influences alcohol seeking.

neuroscience↗

bioRxiv2025

BDH1-Dependent Ketone Body Metabolism Maintains Muller Cell Homeostasis and Retinal Function

Ketone body metabolism serves as an auxiliary regulator of cellular energetics and redox balance, particularly during prolonged fasting and carbohydrate restriction, yet its role in retinal homeostasis under physiological conditions remains poorly defined. {beta}-hydroxybutyrate dehydrogenase 1 (BDH1) is a mitochondrial enzyme that interconverts acetoacetate and {beta}-hydroxybutyrate, and is required for efficient ketone utilization. Here, we investigated the impact of impaired endogenous ketone metabolism on retinal function using global and retinal pigment epithelium (RPE)-specific BDH1 knockout (KO) mice. Global BDH1 KO mice showed reduced circulating {beta}-hydroxybutyrate and blunted fasting-induced ketone elevations, accompanied by ganglion cell loss, structural abnormalities on fundus and OCT imaging, and diminished scotopic and photopic electroretinogram (ERG) a- and b-wave amplitudes, consistent with impaired photoreceptor responses and downstream bipolar and Muller cell signaling. In contrast, RPE-specific BDH1 KO mice exhibited no changes in ERG responses or retinal morphology. Transcriptomic and molecular analyses in global KO retinas revealed disrupted Muller cell homeostasis, including reduced CAMKII-CREB activation, which is required for EAAT1 glutamate transporter expression. Administration of exogenous {beta}-hydroxybutyrate, in vitro and in vivo, restored CAMKII-CREB-EAAT1 signaling, glutamate uptake, and antioxidant gene expression in BDH1 KO mice, demonstrating a central role for ketone bodies in Muller cell metabolic support, glutamate homeostasis, and redox balance. Together with reduced BDH1 expression in human AMD retinas, these findings identify the BDH1-{beta}-hydroxybutyrate axis as a critical metabolic pathway for Muller cell function and retinal integrity, and highlight ketone metabolism as a potential therapeutic target in degenerative retinal diseases.

neuroscience↗

bioRxiv2025

Quantitative spectral Linear Unmixing and Ratiometric FRET for live-cell imaging of protein interactions

We present a biophysical imaging strategy based on linear unmixing Forster resonance energy transfer (lux-FRET) for investigating protein-protein interactions and receptor-mediated signaling in live cells. This method utilizes spectral unmixing of FRET signals acquired via confocal laser scanning microscopy (LSM), enabling high-resolution quantification of molecular interactions with both spatial and temporal precision. Applying lux-FRET, we examined receptor-receptor interactions and downstream signaling events, including agonist specificity for 5-HT receptors. Ratiometric FRET measurements with a genetically encoded cAMP biosensor allowed us to assess biosensor sensitivity to cyclic nucleotides and receptor efficacy. Additionally, we explored physiological interactions between CD44 and 5-HT receptors and characterized the oligomerization state of the 5-HT1A receptor through apparent FRET efficiency analysis. Our findings demonstrate the utility of lux-FRET combined with quantitative molecular microscopy as a powerful tool for dissecting dynamic signaling mechanisms in live cells. This approach offers broad applicability for researchers studying receptor pharmacology, cellular signaling, and protein interaction dynamics. RESEARCH HIGHLIGHTWe present a real-time imaging strategy combining lux-FRET with quantitative molecular microscopy to study protein interactions and receptor signaling in living cells. Using spectral and ratiometric FRET analysis, this method enables high-resolution visualization of dynamic molecular processes under physiological conditions. GRAPHICAL ABSTRACT O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=106 SRC="FIGDIR/small/673709v1_ufig1.gif" ALT="Figure 1"> View larger version (55K): org.highwire.dtl.DTLVardef@42beecorg.highwire.dtl.DTLVardef@4a746org.highwire.dtl.DTLVardef@181f61corg.highwire.dtl.DTLVardef@144d940_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2025

Much higher covariation with foveation timing by superior colliculus than primary visual cortical neuronal activity

The superior colliculus (SC) is a potent driver for orienting movements, but it also possesses short-latency visual responses. Even though such responses largely derive from direct primary visual cortical (V1) input, their relationship to V1 activity has never been analyzed with the same experimental subjects and stimuli. Here, we revisited pioneering observations that trial-by-trial variability in either SC or V1 visual responses may predict eye movement timing variability. We found that V1 covariation with behavioral variability was virtually non-existent in comparison to the SC, whether with respect to visual response onset latency, visual response strength, or pre-stimulus state. By far, our largest predictor of behavioral variability was visual response strength in SC visual-motor neurons. These results suggest that the SC reformats its sensory inputs for exploitation of the SCs proximity to the motor periphery; V1 aids in jumpstarting the sensing process, but the SC much more directly supports visually-driven orienting.

neuroscience↗

bioRxiv2025

Precision Breathing: Asthma Phenotyping via Machine Learning

Asthma is a complex condition characterized by chronic airway inflammation, with varying severity, symptoms, triggers, and treatment responses. Traditional classification relies on clinical attributes, but the growing understanding of asthmas heterogeneity highlights the need for phenotyping. Effective management requires regular monitoring, medication, and prevention of exacerbations, but current diagnostic methods face challenges such as the lack of definitive tests and reliance on subjective measures. Implementing precision medicine, especially for severe cases, necessitates identifying measurable markers in biofluids. This study explores machine learning methods to identify biomarkers differentiating various asthma phenotypic states. We measured inflammatory markers in both plasma and saliva samples and used machine learning algorithms to determine their efficacy in reflecting airway inflammation. Our findings indicate that saliva markers provide a more accurate representation of localized inflammation compared to plasma markers, which reflect a systemic response. Using MRMR (Minimum Redundancy Maximum Relevance) ranking, we enhanced model efficacy. The K-Nearest Neighbor (KNN) classifier achieved 75% accuracy with the first 12 saliva markers, while the Random Forest (RF) classifier performed best for plasma models, though with lower accuracy. Our results suggest machine learning can effectively identify key markers for asthma phenotyping, aiding personalized treatment strategies. Customizable point-of-care devices could validate these models and improve their accuracy, advancing asthma treatment and management.

bioengineering↗

bioRxiv2024

Automated, image-based quantification of peroxisome characteristics with perox-per-cell

perox-per-cell automates cumbersome, image-based data collection tasks often encountered in peroxisome research. The software processes microscopy images to quantify peroxisome features in yeast cells. It uses off-the-shelf image processing tools to automatically segment cells and peroxisomes and then outputs quantitative metrics including peroxisome counts per cell and spatial areas. In validation tests, we found that perox-per-cell output agrees well with manually-quantified peroxisomal counts and cell instances, thereby enabling high-throughput quantification of peroxisomal characteristics. The software is available at https://github.com/AitchisonLab/perox-per-cell

bioinformatics↗

bioRxiv2023

Relationship between luteal size and plasma progesterone concentration in pregnant and non-pregnant Indian crossbred dairy cows

The relationship between luteal size and plasma progesterone concentration in purebred cows has been investigated previously. However, there is limited information on this topic in Indian crossbred cows. This study aimed to evaluate the relationship between luteal size parameters (diameter and area) and plasma progesterone concentration in healthy pregnant and non-pregnant Indian crossbred cows. Fifty healthy lactating crossbred cows were artificially inseminated after estrus detection and retrospectively classified into pregnant (n=29) and non-pregnant (n=21) based on the results of ultrasonographic pregnancy diagnosis. Data on luteal diameter, luteal area, and plasma progesterone concentration collected on Days 7, 14, and 20 in non-pregnant cows and on Days 7, 14, 20, 25, 30, 35, 40, and 60 in pregnant cows were analyzed. Spearmans correlation test was used to evaluate the association between the corpus luteum size parameters and the plasma progesterone concentration. Luteal area was positively correlated with plasma progesterone concentration in both pregnant ({rho}=0.48, P<0.001) and non-pregnant ({rho}=0.43, P=0.001) cows. Luteal diameter had a relatively weaker correlation with plasma progesterone concentration in both pregnant ({rho}=0.45, P<0.001) and non-pregnant ({rho}=0.24, P=0.058) cows. These results suggest that luteal area is a better indicator of CL function than luteal diameter in healthy Indian crossbred cows.

physiology↗

bioRxiv2023

A bioorthogonal antibody-based chemically-induced-dimerization switch for therapeutic application

We present the Indinavir Ligand Induced Transient Engagement switch (IDV LITE Switch), a fully synthetic Chemically Induced Dimerization (CID) system wherein two humanized antibody fragments are heterodimerized by the antiviral drug indinavir. The IDV LITE Switch represents the first CID system made from fully humanized protein components and dimerized by a clinically approved small molecule drug lacking a mammalian target, making it an ideal bioorthogonal molecular switch for application in small-molecule controlled therapeutics.

synthetic biology↗

bioRxiv2022

Single session of rTMS enhances brain metastability and intrinsic ignition

BackgroundEmerging evidence support the view that brain stimulation might improve essential tremor (ET) by altering brain networks and facilitating plasticity. Yet, we are still missing a mechanistic explanation of the whole brain dynamics underlying these plasticity defining changes. MethodIn this study, we explored the effect of low-frequency repetitive transcranial magnetic stimulation (rTMS) over left primary motor cortex (L-M1) on functional connectivity dynamics (FCD) in patients with ET. Resting-state fMRI (RsfMRI) was acquired before and after a single session of rTMS in 30 patients with ET and compared with RsfMRI of 20 age and gender matched healthy controls (HCs). We have measured the effect of brain stimulation using network topological re-organization through whole brain integration and segregation, brain stability and capacity of neural propagation through metastability and intrinsic ignition. ResultsPatients with ET had altered FCD measures compared to controls. After a single session rTMS, the brain connectivity measures approached normality and patients with ET revealed significantly higher integration, lower segregation with higher metastability and increased intrinsic ignition. ConclusionBrain metastability and intrinsic ignition measures could be valuable tools in appreciating mechanisms of brain stimulation in ET and other neurological diseases.

neuroscience↗

bioRxiv2022

Deep attention based variational autoencoder for antimicrobial peptide discovery

Antimicrobial peptides (AMPs) have been proposed as a potential solution against multiresistant pathogens. Designing novel AMPs requires exploration of a vast chemical space which makes it a challenging problem. Recently natural language processing and generative deep learning have shown great promise in exploring the vast chemical space and generating new chemicals with desired properties. In this study we leverage a variational attention mechanism in the generative variational autoencoder where attention vector is also modeled as a latent vector. Variational attention helps with the diversity and quality of the generated AMPs. The generated AMPs from this model are novel, have high statistical fidelity and have similar physicochemical properties such as charge, hydrophobicity and hydrophobic moment to the real to the real antimicrobial peptides.

bioinformatics↗

bioRxiv2022

Probing single cell fermentation flux and intercellular exchange networks via pH-microenvironment sensing and inverse modeling

The homeostatic control of their environment is an essential task of living cells. It has been hypothesized that when microenvironmental pH inhomogeneities are induced by high cellular metabolic activity, diffusing protons act as signaling molecules, driving the establishment of cross-feeding networks sustained by the cell-to-cell shuttling of overflow products such as lactate. Despite their fundamental role, the extent and dynamics of such networks is largely unknown due to the lack of methods in single cell flux analysis. In this study we provide direct experimental characterization of such exchange networks. We devise a method to quantify single cell fermentation fluxes over time by integrating high-resolution pH microenvironment sensing via ratiometric nanofibers with constraint-based inverse modeling. We apply our method to cell cultures with mixed populations of cancer cells and fibroblasts. We find that the proton trafficking underlying bulk acidification is strongly heterogeneous, with maximal single cell fluxes exceeding typical values by up to 3 orders of magnitude. In addition, a crossover in time from a networked phase sustained by densely connected "hubs" (corresponding to cells with high activity) to a sparse phase dominated by isolated dipolar motifs (i.e. by pair-wise cell-to-cell exchanges) is uncovered, which parallels the time course of bulk acidification. Our method promises to shed light on issues ranging from the homeostatic function of proton exchange to the metabolic coupling of cells with different energetic demands, and paves the way for real-time non-invasive single cell metabolic flux analysis.

biophysics↗

bioRxiv2022

Protein kinase D promotes prostate cancer cell bone metastasis by positively regulating Runx2 in a MEK/ERK1/2-dependent manner

Most cancer patients die because of tumor metastasis not due to tumors at the primary site. Prostate tumors in advance stages frequently metastasize to the bone, which is the main cause of death for the disease. The family of protein kinase D (PKD) has been implicated in prostate cancer development, however, its role in prostate cancer metastasis has not been investigated. In this study, we examined the contribution of PKD to the metastatic potential of prostate cancer cells and the impact of PKD inhibition on prostate cancer bone metastasis in vivo. Our data showed that depletion of PKDs by siRNA or inhibition of PKD by an inhibitor CRT0066101 in a highly invasive prostate cancer PC3-ML cells potently inhibited colony formation and cell migration. Furthermore, depletion or inhibition of PKD significantly blocked invasion of PC3-ML cells and suppressed expression of genes related to bone metastasis. The reduced invasive activity resulted from PKD depletion was in part mediated through the transcription factor Runx2 as its silencing decreased PKD-mediated metastatic gene expression. Mechanistically, our data indicate that PKD modulated Runx2 target gene expression through the MEK/ERK1/2 signaling axis. Additionally, we examined whether PKD inhibitor CRT0066101 could prevent prostate cancer bone metastasis in a mouse model of metastasis, where intracardiac injection of PC3-ML cells led to metastasis of cells to the bone. We found that CRT0066101 potently decreased the frequency of micrometastases in mouse bone. These results indicate that PKDs play an important role in bone metastasis of prostate cancer cells and its inhibition may be beneficial for treatment of advanced stages of cancer.

cancer biology↗

bioRxiv2021

SPECT/CT imaging, biodistribution and radiation dosimetry of a 177Lu-DOTA-integrin αvβ6 cystine knot peptide in a pancreatic cancer xenograft model

IntroductionPancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignant neoplasms, as many cases go undetected until they reach an advanced stage. Integrin v{beta}6 is a cell surface receptor overexpressed in PDAC. Consequently, it may serve as a target for the development of probes for imaging diagnosis and radioligand therapy. Engineered cystine knottin peptides specific for integrin v{beta}6 have recently been developed showing high affinity and stability. This study aimed to evaluate an integrin v{beta}6-specific knottin molecular probe containing the therapeutic radionuclide 177Lu for targeting of PDAC. MethodsThe expression of integrin v{beta}6 in PDAC cell lines BxPC3 and Capan2 was analyzed using RT-qPCR and immunofluorescence. In vitro competition and saturation radioligand binding assays were performed to calculate the binding affinity of the DOTA-coupled tracer loaded with and without lutetium to BxPC3 and Capan2 cell lines. To evaluate tracer accumulation in the tumor and organs, SPECT/CT, biodistribution and dosimetry projections were carried out using a Capan2 xenograft tumor mouse model. ResultsRT-qPCR and immunofluorescence results showed high expression of integrin v{beta}6 in BxPC3 and Capan2 cells. A competition binding assay revealed high affinity of the tracer with IC50 values of 1.69 nM and 9.46 nM for BxPC3 and Capan2, respectively. SPECT/CT and biodistribution analysis of the conjugate 177Lu-DOTA-integrin v{beta}6 knottin demonstrated accumulation in Capan2 xenograft tumors (3.13 {+/-} 0.63 %IA/g at day 1 post injection) with kidney uptake at 19.2 {+/-} 2.5 %IA/g, declining much more rapidly than in tumors. Conclusion177Lu-DOTA-integrin v{beta}6 knottin was found to be a high-affinity tracer for PDAC tumors with considerable tumor accumulation and moderate, rapidly declining kidney uptake. These promising results warrant a preclinical treatment study to establish therapeutic efficacy.

cancer biology↗