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Filizola, M.

Publications and source records attributed to Filizola, M..

At least 19 recordsLinked to original sources

Transition Intermediates Encode Ligand Efficacy at the μ-Opioid Receptor-Gi Protein Complex

How ligands with different efficacies regulate G protein-coupled receptor signaling remains incompletely understood. Here, we combine Markov state modeling of nearly one millisecond of aggregate all-atom molecular dynamics simulations with time-resolved cryogenic-electron microscopy (cryo-EM) to reconstruct the most probable transition pathways connecting recently resolved structures of guanosine triphosphate (GTP)-bound -opioid receptor (MOR)-Gi1 complexes with the full agonist lofentanil (LFT) or partial agonist mitragynine pseudoindoxyl (MP). The models predict four previously unresolved intermediate conformations. Guided by these predictions, reanalysis of the cryo-EM particle ensemble identifies conformational populations consistent with all four intermediates. Remarkably, the largest ligand-dependent structural differences emerge within these intermediates rather than in the previously resolved states. LFT favors a predominantly sequential and kinetically efficient transition pathway, whereas MP stabilizes a broader intermediate ensemble along this pathway and slows progression toward later states. Together, these complementary approaches provide an enriched thermodynamic and kinetic description of MOR-mediated G protein activation, revealing that opioid efficacy is encoded, at least in part, in the differential stabilization and kinetics of transition intermediates extending beyond GTP binding but well before complete G protein dissociation.

biophysics↗

Mechanistic Basis for the Selective Recognition of the Fcγ Receptor IIa by Monoclonal Antibody IV.3

The monoclonal antibody IV.3 selectively binds the platelet Fc{gamma} receptor IIa (Fc{gamma}RIIa), potently blocking immune complex engagement without cross-reacting with the closely-related Fc{gamma}RIIb. This specificity has made IV.3 invaluable for dissecting Fc{gamma}RIIa-mediated activation in diverse conditions, including infection, autoimmunity, thromboinflammation, and platelet-mediated thrombosis. We combined cryogenic electron microscopy, surface plasmon resonance, alchemical free energy calculations, and molecular dynamics simulations to elucidate IV.3s binding sites on Fc{gamma}RIIa and the mechanistic basis of IV.3 specificity. We find that IV.3 engages a broader Fc{gamma}RIIa epitope than previously recognized, extending beyond residues H/R134 and L135 (R and S in Fc{gamma}RIIb). Simulations of Fc{gamma}IIa-R134 variants bearing either L135 or S135 reveal that IV.3 specificity arises from hydrophobic stabilization mediated by L135 and disruption of an R134-specific interaction network in the presence of S135. These findings provide a mechanistic framework for rational design of Fc{gamma}RIIa-targeted therapeutics.

biophysics↗

Structural and dynamic studies uncover a distinct allosteric modulatory site at the mu-opioid receptor

Positive allosteric modulators (PAMs) of the opioid receptor (MOR) offer a promising path toward safer opioid therapeutics, yet their mechanisms of action remain poorly understood. Here, we uncover the structural and mechanistic basis of BMS-986187, a chemically distinct MOR PAM with in vivo efficacy, using an integrated approach combining cryogenic electron microscopy (cryo-EM), molecular dynamics (MD) simulations, signaling assays, and site-directed mutagenesis. We identify a previously uncharacterized allosteric site for BMS-986187, a lipid-facing pocket formed by MOR transmembrane helices 2, 3, and 4, distinct from sites occupied by other known MOR PAMs or negative allosteric modulators. BMS-986187 engages both receptor residues and a neighboring cholesterol molecule, suggesting a cooperative ligand-lipid mechanism. Our studies pinpoint residues essential for allosteric modulation, while information-theory analysis of MD trajectories uncovers specific allosteric communication pathways linking the PAM site to both the orthosteric agonist DAMGO and the G protein interface. Together, these findings redefine the landscape of MOR allosteric modulation by revealing a novel binding site, a potentially lipid-sensitive allosteric mechanism, and the molecular wiring of long-range communication within MOR. This work provides a new molecular framework for the rational design of PAMs targeting opioid receptors with improved precision and possible therapeutic potential.

pharmacology and toxicology↗

BOLD-GPCRs: A Transformer-Powered App for Predicting Ligand Bioactivity and Mutational Effects Across Class A GPCRs

G protein-coupled receptors (GPCRs) are important targets for drug discovery owing to their ability to respond to a broad range of stimuli and their involvement in numerous pathologies. Although traditional ligand-based and structure-based approaches have facilitated the development of effective therapeutics for many GPCRs, these approaches often fall short when applied to receptors with limited ligand or structural data. This limitation highlights the critical need for advanced strategies capable of accurately predicting ligand bioactivity across the entire GPCR family, especially for understudied receptor subtypes. In this study, we introduce BOLD-GPCRs (BERT-Optimized Ligand Discovery for GPCRs), a deep learning framework designed to enhance the prediction of ligand bioactivity across class A GPCRs. Accessible via a user-friendly web interface, BOLD-GPCRs employs transfer learning and leverages curated datasets of known class A GPCR ligands, receptor sequences, and signaling-relevant mutations. By integrating dense neural network classifiers with transformer-based protein language models, BOLD-GPCRs captures complex relationships between receptor sequence/function and ligand activity. Our results demonstrate that BOLD-GPCRs achieves robust predictive performance for both ligand bioactivity and mutational effects across a broad range of class A GPCRs, underscoring its potential as a valuable tool for ligand discovery, especially for poorly characterized receptors. For Table of Contents Use OnlyBOLD-GPCRs: A Transformer-Powered App for Predicting Ligand Bioactivity and Mutational Effects Across Class A GPCRs Davide Provasi, Kirill Konovalov, Nicholas Riina, Olivia Cullen, and Marta Filizola O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=94 SRC="FIGDIR/small/668547v1_ufig1.gif" ALT="Figure 1"> View larger version (16K): org.highwire.dtl.DTLVardef@2026bborg.highwire.dtl.DTLVardef@cec535org.highwire.dtl.DTLVardef@f52438org.highwire.dtl.DTLVardef@1cfbe6_HPS_FORMAT_FIGEXP M_FIG C_FIG

bioinformatics↗

Fine-Tuned Deep Transfer Learning Models for Large Screenings of Safer Drugs Targeting Class A G Protein-Coupled Receptors

G protein-coupled receptors (GPCRs) remain a focal point of research due to their critical roles in cell signaling and their prominence as drug targets. However, directly linking drug efficacy to receptor-mediated activation of specific intracellular transducers and the resulting physiological outcomes remains challenging. It is unclear whether the enhanced therapeutic window of certain drugs -- defined as the dose range that provides effective therapy with minimal side effects -- stems from their low intrinsic efficacy across all signaling pathways or ligand bias, wherein specific transducer subtypes are preferentially activated in a given cellular system compared to a reference ligand. Accurately predicting safer compounds, whether through low intrinsic efficacy or ligand bias, would greatly advance drug development. While AI models hold promise for such predictions, the development of deep learning models capable of reliably forecasting GPCR ligands with defined bioactivities remains challenging, largely due to the limited availability of high-quality data. To address this, we pre-trained a model on receptor sequences and ligand datasets across all class A GPCRs, and then refined it to predict low-efficacy compounds or biased agonists for individual class A GPCRs. This was achieved using transfer learning and a neural network incorporating natural language processing of target sequences and receptor mutation effects on signaling. These two fine-tuned models--one for low-efficacy agonists and one for biased agonists--are available on demand for each class A GPCR and enable virtual screening of large chemical libraries, thereby facilitating the discovery of compounds with potentially improved safety profiles.

bioinformatics↗

Structural basis for saxitoxin congener binding and neutralization by anuran saxiphilins

Dinoflagellates and cyanobacteria in harmful red tide algal blooms produce saxitoxin (STX) and [~]50 congeners that block voltage-gated sodium channel (NaV) function and disrupt bioelectrical signals1-4. Consuming seafood carrying these lethal toxins causes paralytic shellfish poisoning (PSP), a growing public health hazard due to climate change5-7 that motivates efforts to detect these toxins and counteract their noxious effects. Although structural studies of NaVs8,9 and anuran soluble STX binding proteins known as saxiphilins (Sxphs)10,11 revealed convergent binding modes for the bis-guanidinium STX core10,11, the structural basis for STX congener recognition is unknown. Here, we show that American bullfrog (Rana catesbeiana) RcSxph10,11 and High Himalaya frog (Nanorana parkeri) NpSxph10 use a pre-organized pocket to sequester STX congeners through a binding mode shared with STX. This lock and key recognition yields a tradeoff between a relatively rigid high-affinity toxin binding site in which bound waters are crucial and the ability of Sxphs to accommodate STX congener modifications. Importantly, functional studies show that Sxphs act as toxin sponges that reverse NaV block by multiple STX congeners and can detect these bis-guanidinium toxins in a radioligand receptor binding assay (RBA) for PSP toxin environmental testing12,13. Our findings establish how Sxphs sequester diverse neurotoxins and reveal structural factors underlying STX congener binding differences between Sxphs and NaVs that are rooted in the distinct toxin binding orientations on these two targets. These insights expand the molecular foundation required for understanding toxin sponge action and for guiding development of new means to monitor PSTs and mitigate their harmful effects.

biophysics↗

Burkholderia cenocepacia epigenetic regulator M.BceJIV simultaneously engages two DNA recognition sequences for methylation

Burkholderia cenocepacia is an opportunistic and infective bacterium containing an orphan DNA methyltransferase (M.BceJIV) with roles in regulating gene expression and motility of the bacterium. M.BceJIV recognizes a GTWWAC motif (where W can be an adenine or a thymine) and methylates the N6 of the adenine at the fifth base position (GTWWAC). Here, we present a high-resolution crystal structure of M.BceJIV/DNA/sinefungin ternary complex and allied biochemical, computational, and thermodynamic analyses. Remarkably, the structure shows not one, but two DNA substrates bound to the M.BceJIV dimer, wherein each monomer contributes to the recognition of two recognition sequences. This unexpected mode of DNA binding and methylation has not been observed previously and sets a new precedent for a DNA methyltransferase. We also show that methylation at two recognition sequences occurs independently, and that GTWWAC motifs are enriched in intergenic regions of a strain of B. cenocepacias genome. We further computationally assess the interactions underlying the affinities of different ligands (SAM, SAH, and sinefungin) for M.BceJIV, as a step towards developing selective inhibitors for limiting B. cenocepacia infection.

biophysics↗

Structural Insights into the Unexpected Agonism of Tetracyclic Antidepressants at Serotonin Receptors 5-HT1eR and 5-HT1FR

Serotonin (5-hydroxytryptamine, 5-HT) acts via 13 different receptors in humans. Of these receptor subtypes, all but 5-HT1eR have confirmed roles in native tissue and are validated drug targets. Despite 5-HT1eRs therapeutic potential and plausible druggability, the mechanisms of its activation remain elusive. To illuminate 5-HT1eRs pharmacology in relation to the highly homologous 5-HT1FR, we screened a library of aminergic receptor ligands at both receptors and observe 5-HT1e/1FR agonism by multicyclic drugs described as pan-antagonists at 5-HT receptors. Potent agonism by tetracyclic antidepressants mianserin, setiptiline, and mirtazapine suggests a mechanism for their clinically observed anti-migraine properties. Using cryoEM and mutagenesis studies, we uncover and characterize unique agonist-like binding poses of mianserin and setiptiline at 5-HT1eR distinct from similar drug scaffolds in inactive-state 5-HTR structures. Together with computational studies, our data suggest that these binding poses alongside receptor-specific allosteric coupling in 5-HT1eR and 5-HT1FR contribute to the agonist activity of these antidepressants.

neuroscience↗

Structural basis of allosteric modulation ofmetabotropic glutamate receptor activation and desensitization

The metabotropic glutamate receptors (mGluRs) are neuromodulatory family C G protein coupled receptors which assemble as dimers and allosterically couple extracellular ligand binding domains (LBDs) to transmembrane domains (TMDs) to drive intracellular signaling. Pharmacologically, mGluRs can be targeted either at the LBDs by glutamate and synthetic orthosteric compounds or at the TMDs by allosteric modulators. Despite the potential of allosteric TMD-targeting compounds as therapeutics, an understanding of the functional and structural basis of their effects on mGluRs is limited. Here we use a battery of approaches to dissect the distinct functional and structural effects of orthosteric versus allosteric ligands. We find using electrophysiological and live cell imaging assays that both agonists and positive allosteric modulators (PAMs) can drive activation and desensitization of mGluRs. The effects of PAMs are pleiotropic, including both the ability to boost the maximal response to orthosteric agonists and to serve independently as desensitization-biased agonists across mGluR subtypes. Conformational sensors reveal PAM-driven inter-subunit re-arrangements at both the LBD and TMD. Motivated by this, we determine cryo-electron microscopy structures of mGluR3 in the presence of either an agonist or antagonist alone or in combination with a PAM. These structures reveal PAM-driven re-shaping of intra- and inter-subunit conformations and provide evidence for a rolling TMD dimer interface activation pathway that controls G protein and beta-arrestin coupling. Highlights-Agonists and PAMs drive mGluR activation, desensitization, and endocytosis -PAMs are desensitization-biased and synergistic with agonists -Four combinatorial ligand conditions reveal an ensemble of full-length mGluR structures with novel interfaces -Activation and desensitization involve rolling TMD interfaces which are re-shaped by PAM

biophysics↗

Enhancing Opioid Bioactivity Predictions through Integration of Ligand-Based and Structure-Based Drug Discovery Strategies with Transfer and Deep Learning Techniques

The opioid epidemic has cast a shadow over public health, necessitating immediate action to address its devastating consequences. To effectively combat this crisis, it is crucial to discover better opioid drugs with reduced addiction potential. Artificial intelligence-based and other machine learning tools, particularly deep learning models, have garnered significant attention in recent years for their potential to advance drug discovery. However, utilizing these tools poses challenges, especially when training samples are insufficient to achieve adequate prediction performance. In this study, we investigate the effectiveness of transfer learning using combined ligand-based and structure-based molecular descriptors from the entire opioid receptor (OR) subfamily in building robust deep learning models for enhanced bioactivity prediction of opioid ligands at each individual OR subtype. Our studies hold the potential to greatly advance opioid research by enabling the rapid identification of novel chemical probes with specific bioactivities, which can aid in the study of receptor function and contribute to the future development of improved opioid therapeutics.

bioinformatics↗

De Novo Design of κ-Opioid Receptor Antagonists Using a Generative Deep Learning Framework

Likely effective pharmacological interventions for the treatment of opioid addiction include attempts to attenuate brain reward deficits during periods of abstinence. Pharmacological blockade of the {kappa}-opioid receptor (KOR) has been shown to abolish brain reward deficits in rodents during withdrawal, as well as to reduce the escalation of opioid use in rats with extended access to opioids. Although KOR antagonists represent promising candidates for the treatment of opioid addiction, very few potent selective KOR antagonists are known to date and most of them exhibit significant safety concerns. Here, we used a generative deep learning framework for the de novo design of chemotypes with putative KOR antagonistic activity. Molecules generated by models trained with this framework were prioritized for chemical synthesis based on their predicted optimal interactions with the receptor. Our models and proposed training protocol were experimentally validated by binding and functional assays.

bioinformatics↗

Gαs slow conformational transition upon GTP binding and a novel Gαs regulator

G proteins are major signaling partners for G protein-coupled receptors (GPCRs). Although stepwise structural changes during GPCR-G protein complex formation and guanosine diphosphate (GDP) release have been reported, no information is available with regard to guanosine triphosphate (GTP) binding. Here, we used a novel Bayesian integrative modeling framework that combines data from hydrogen-deuterium exchange mass spectrometry, tryptophan-induced fluorescence quenching, and metadynamics simulations to derive a kinetic model and atomic-level characterization of stepwise conformational changes incurred by the {beta}2-adrenergic receptor ({beta}2AR)-Gs complex after GDP release and GTP binding. Our data suggest rapid GTP binding and GTP-induced dissociation of Gs from {beta}2AR and G{beta}{gamma}, as opposed to a slow closing of the Gs -helical domain (AHD). Yeast-two-hybrid screening using Gs AHD as bait identified melanoma-associated antigen D2 (MAGE D2) as a novel AHD-binding protein, which was also shown to accelerate the GTP-induced closing of the Gs AHD.

molecular biology↗

A Promising Chemical Series of Positive Allosteric Modulators of the μ-Opioid Receptor that Enhance the Antinociceptive Efficacy of Opioids but not their Adverse Effects

Positive allosteric modulators (PAMs) of the {micro}-opioid receptor (MOR) have been proposed to exhibit therapeutic potential by maximizing the analgesic properties of clinically used opioid drugs while limiting their adverse effects or risk of overdose as a result of using lower drug doses. We herein report in vitro and in vivo characterization of two small molecules from a chemical series of MOR PAMs that exhibit: (i) MOR PAM activity and receptor subtype selectivity in vitro, (ii) a differential potentiation of the antinociceptive effect of oxycodone, morphine, and methadone in mouse models of pain that roughly correlates with in vitro activity, and (iii) a lack of potentiation of adverse effects associated with opioid administration, such as somatic withdrawal, respiratory depression, and analgesic tolerance. This series of MOR PAMs holds promise for the development of adjuncts to opioid therapy to mitigate against overdose and opioid use disorders.

neuroscience↗

A novel mitragynine analog with low efficacy mu-opioid receptor agonism displays antinociception with attenuated adverse effects

Dried kratom leaves are anecdotally used for the treatment of pain, opioid dependence, and alcohol use disorder. We have previously shown that kratoms natural products (mitragynine) and semi-synthetic analogs (7-hydroxy mitragynine (7OH) and mitragynine pseudoindoxyl) are mu opioid receptor (MOR) agonists that show minimal {beta}-arrestin2 recruitment. To further investigate the structure activity relationships of G-protein potency, efficacy, and {beta}-arrestin2 recruitment, we diversified the mitragynine/7OH templates at the C9, -10 and -12 positions of the aromatic ring of the indole moiety. Three lead C9 analogs, synthesized by swapping the 9-methoxy group with varied substituents, namely phenyl (SC11), methyl (SC12), 3-furanyl (SC13), were further characterized using a panel of in vitro and ex vivo electrophysiology assays. All three compounds were partial agonists with lower efficacy than both DAMGO and morphine in heterologous G-protein assays and synaptic physiology. SC11-13 also showed lower recruitment of both {beta}-arrestin subtypes compared to DAMGO, and in assays with limited MOR receptor reserve, the G-protein efficacy of SC11, SC12 and SC13 was comparable to buprenorphine. In mouse models, at equianalgesic doses SC13 showed MOR-dependent analgesia with potency similar to morphine without respiratory depression, hyperlocomotion, constipation, or place conditioning. Taken together, these results suggest that MOR agonists with a G-protein efficacy profile similar to buprenorphine can be developed into opioids that are effective analgesics with greatly reduced liabilities.

pharmacology and toxicology↗

Differences in interactions between transmembrane domains tune the activation of metabotropic glutamate receptors

The metabotropic glutamate receptors (mGluRs) form a family of neuromodulatory G protein-coupled receptors that contain both a seven-helix transmembrane domain (TMD) and a large extracellular ligand-binding domain (LBD) which enables stable dimerization. While numerous studies have revealed variability across subtypes in the initial activation steps at the level of LBD dimers, an understanding of inter-TMD interaction and rearrangement remains limited. Here we use a combination of single molecule fluorescence, molecular dynamics, functional assays, and conformational sensors to reveal that distinct TMD assembly properties drive differences between mGluR subtypes. We uncover a variable region within transmembrane helix 4 (TM4) that contributes to homo- and heterodimerization in a subtype-specific manner and tunes orthosteric, allosteric and basal activation. We also confirm a critical role for a conserved inter-TM6 interface in stabilizing the active state during orthosteric or allosteric activation. Together this study informs a working model of inter-TMD rearrangement that drives mGluR function.

neuroscience↗

High-resolution Structures of multiple 5-HT3AR-setron complexes reveal a novel mechanism of competitive inhibition

Serotonin receptors (5-HT3AR) play a crucial role in regulating gut movement, and are the principal target of setrons, a class of high-affinity competitive antagonists, used in the management of nausea and vomiting associated with radiation and chemotherapies. Structural insights into setron-binding poses and their inhibitory mechanisms are just beginning to emerge. Here, we present high-resolution cryo-EM structures of full-length 5-HT3AR in complex with palonosetron, ondansetron, and alosetron. Each structure reveals a distinct interaction fingerprint between the setron and binding-pocket residues that may underlie their diverse affinities. In addition, setrons elicit varying degrees of conformational change throughout the channel that, quite surprisingly, lie along the channel activation pathway, suggesting a novel mechanism of competitive inhibition. Molecular dynamic simulations were used to assess binding-poses and the drug-target interaction dynamics. Together, this study provides a molecular basis for setron binding affinities and their inhibitory effects.

biophysics↗

Mechanism of μ-Opioid Receptor-Magnesium Interaction and Positive Allosteric Modulation.

In the era of opioid abuse epidemics, there is an increased demand for understanding how opioid receptors can be allosterically modulated to guide the development of more effective and safer opioid therapies. Among the modulators of the {micro}-opioid (MOP) receptor, which is the pharmacological target for the majority of clinically used opioid drugs, are monovalent and divalent cations. Specifically, the monovalent sodium cation (Na+) has been known for decades to affect MOP receptor signaling by reducing agonist binding, whereas the divalent magnesium cation (Mg2+) has been shown to have the opposite effect, notwithstanding the presence of sodium chloride. While ultra-high resolution opioid receptor crystal structures have revealed a specific Na+ binding site and molecular dynamics (MD) simulation studies have supported the idea that this monovalent ion reduces agonist binding by stabilizing the receptor inactive state, the putative binding site of Mg2+ on the MOP receptor, as well as the molecular determinants responsible for its positive allosteric modulation of the receptor, are unknown. In this work, we carried out tens of microseconds of all-atom MD simulations to investigate the simultaneous binding of Mg2+ and Na+ cations to inactive and active crystal structures of the MOP receptor embedded in an explicit lipid/water environment. Analyses of these simulations shed light on (a) the preferred binding sites of Mg2+ on the MOP receptor, (b) details of the competition between Mg2+ and Na+ cations for specific sites, (c) estimates of binding affinities, and (d) testable hypotheses of the molecular mechanism underlying the positive allosteric modulation of the MOP receptor by the Mg2+ cation.\n\nStatement of SignificanceOverprescription of opioid drugs in the late 1990s, followed by abuse of both prescription and illicit opioid drugs, has led to what is nowadays called \"opioid overdose crisis\" or \"opioid epidemic\", with more than 130 Americans dying daily from opioid overdose at the time of writing. To reduce opioid doses, and thereby prevent or treat overdose and opioid use disorders, attention has recently shifted to the use of co-analgesics. Understanding how opioid receptor targets can be allosterically modulated by these elements, including cations, is key to the development of improved therapeutics. Here, we provide an atomic-level understanding of the mechanism by which magnesium binds to the {micro}-opioid receptor and enhances opioid drug efficacy by stabilizing the receptor activated state.

biophysics↗

Novel Pure αVβ3 Integrin Antagonists That Do Not Induce Receptor Extension, Prime the Receptor, or Enhance Angiogenesis at Low Concentrations

The integrin V{beta}3 receptor has been implicated in several important diseases, but no V{beta}3 antagonists are approved for human therapy. One possible limitation of current small-molecule antagonists is their ability to induce a major conformational change in the receptor that induces it to adopt a high-affinity ligand-binding state. In response, we used structural inferences from a pure peptide antagonist to design the small-molecule pure antagonists TDI-4161 and TDI-3761. Both compounds inhibit V{beta}3-mediated cell adhesion to V{beta}3 ligands, but do not induce the conformational change as judged by antibody binding, electron microscopy, X-ray crystallography, and receptor priming studies. Both compounds demonstrated the favorable property of inhibiting bone resorption in vitro, supporting potential value in treating osteoporosis. Neither, however, had the unfavorable property of the V{beta}3 antagonist cilengitide of paradoxically enhancing aortic sprout angiogenesis at concentrations below its IC50, which correlates with cilengitides enhancement of tumor growth in vivo.\n\nSignificance StatementV{beta}3 is a potential therapeutic target for several important human diseases, but there are currently no V{beta}3 antagonists approved for human therapy. Current candidates are primarily based on the Arg-Gly-Asp (RGD) motif and act as partial agonists in that they induce V{beta}3 to undergo a conformational change that converts it into a high-affinity ligand-binding state. We have used structure-guided design to produce pure small-molecule V{beta}3 antagonists that do not induce the conformational change as judged by protein crystallography, electron microscopy, and receptor priming. These compounds inhibit V{beta}3-mediated bone resorption in vitro, but unlike the partial agonist cilengitide, do not enhance angiogenesis at low doses, a property that correlates with low-dose cilengitides enhancement of tumor growth in vivo. These pure V{beta}3 antagonists can help define V{beta}3s role in animal models. If they demonstrate benefits over partial agonists in these model systems, they may be appropriate to consider for human therapy.

pharmacology and toxicology↗