Journal: International journal of molecular sciences

Article Title: Long Chain N3-PUFA Decreases ACE2 Protein Levels and Prevents SARS-CoV-2 Cell Entry.

doi: 10.3390/ijms232213825

Figure Lengend Snippet: Figure 1. DHA reduces both ACE1 and ACE2 levels in key rat tissues. Western blotting was used to measure ACE1 and ACE2 levels relative to total protein load, as

Article Snippet: Rabbit anti-ACE2 polyclonal primary antibody (Catalog #: 3217, ProSci, San Diego, CA, USA) and StarBright Blue 700 Goat Anti-Rabbit secondary antibody (Catalog#: 12004162, Bio-Rad, Hercules, CA, USA) were used to detect ACE2.

Techniques: Western Blot

Journal: International journal of molecular sciences

Article Title: Long Chain N3-PUFA Decreases ACE2 Protein Levels and Prevents SARS-CoV-2 Cell Entry.

doi: 10.3390/ijms232213825

Figure Lengend Snippet: Figure 2. DHA differentially modulates ACE1 and ACE2 levels in growing and quiescent EA.hy926 en- dothelial cells. Western blotting was used to compare ACE1 and ACE2 relative to total protein load, as measured by Ponceau S in growing cells treated with ALA, EPA, or DHA at the indicated concentrations (µM) for (a) 8 and (b) 24 h, as well as in quiescent cells treated with n3-PUFA for (c) 8 and (d) 24 h. The band intensities of ACE2 and ACE1 were quantified and are graphically presented in panels (e,f), respectively; the 100 kDa band (grey bars) represents non-glycosylated ACE2, whereas the 130 kDa band (black bars) corresponds to N-glycosylated ACE2. Data are presented as mean ± SEM, n = 3; bars not sharing a common letter in the graphs are significantly different (p < 0.05) based on Duncan’s multiple range or LSD post-hoc tests.

Article Snippet: Rabbit anti-ACE2 polyclonal primary antibody (Catalog #: 3217, ProSci, San Diego, CA, USA) and StarBright Blue 700 Goat Anti-Rabbit secondary antibody (Catalog#: 12004162, Bio-Rad, Hercules, CA, USA) were used to detect ACE2.

Techniques: Western Blot

Journal: International journal of molecular sciences

Article Title: Long Chain N3-PUFA Decreases ACE2 Protein Levels and Prevents SARS-CoV-2 Cell Entry.

doi: 10.3390/ijms232213825

Figure Lengend Snippet: Figure 5. Schematic of proposed mechanism of action. LCn3-PUFAs, EPA and DHA, reduce ACE2 protein levels. These n3-PUFAs may also decrease ACE2 glycosylation. These mechanisms may explain how DHA blocks SARS-CoV-2 pseudovirus entry into HEK293 cells. LCn3-PUFAs also downregulate ACE1 protein levels, thus maintaining the balance between ACE1 and ACE2, and diminishing the risk of adverse CVD outcomes. This figure was prepared by S. Huang using Microsoft PowerPoint software version 16.16.27.

Article Snippet: Rabbit anti-ACE2 polyclonal primary antibody (Catalog #: 3217, ProSci, San Diego, CA, USA) and StarBright Blue 700 Goat Anti-Rabbit secondary antibody (Catalog#: 12004162, Bio-Rad, Hercules, CA, USA) were used to detect ACE2.

Techniques: Glycoproteomics, Software

Journal: iScience

Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

doi: 10.1016/j.isci.2024.109330

Figure Lengend Snippet: A large fraction of serum sACE2 is inactive and binds the SARS-CoV-2 spike (A) ACE2 was pulled down from indicated volumes of serum from patients and HDs using RBD-coupled beads. Recombinant ACE2 (rACE2) was loaded as control. Markers (M) in kDa. ∗Unspecific bands. (B) Specificity confirmed by a mutant RBD (A475R/G496R) lacking ACE2 binding and by an HIV gp140 control. (C) Percent inhibition (%) of 50 ng/mL rACE2 after addition to serum plotted against a-sACE2. Significance indicates a likelihood ratio test to compare a two-degree polynomial model with linear regression for moderate or severe COVID-19. (D) Activity of rACE2 spike-in (%) determined in serum fractions collected after ultrafiltration with indicated cut-off values. (E) Determination of a-sACE2 in indicated reciprocal serum dilutions. (F) Pearson correlation with a 95% confidence interval of a-sACE2 in undiluted samples and maximum a-sACE2 detected after serum dilution. (C), (E), and (F) include measurements of repeated longitudinal blood drawings. For gel source data, see Figure S11 .

Article Snippet: Anti-human ACE2 antibody 3215 , ProSci Incorporated , #3215.

Techniques: Recombinant, Control, Mutagenesis, Binding Assay, Inhibition, Activity Assay

Journal: iScience

Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

doi: 10.1016/j.isci.2024.109330

Figure Lengend Snippet: Serology suggests that sACE2 impairs generation of antibodies preventing RBD-ACE2 interaction (A) Scheme depicting SARS-CoV-2 spike epitope masking by sACE2. (B) Serum IgG binding to RBD (ED50, serum dilution corresponding to 50% of maximum binding activity) of HDs (blue, N = 151), moderate (yellow, N = 120) and severe (red, N = 198) patients collected >20 PSO. Patients are stratified into the respective WHO class at the time of sampling. Statistical analyses by two-sided Mann–Whitney test (∗∗∗∗p < 0.0001, ∗∗∗p < 0.001, ∗∗p < 0.01, and ∗p < 0.05; ns, not significant). Boxplots depict median +/− interquartile range. Whisker length is 1.5 interquartile ranges. (C) Blocking of ACE2-RBD interaction (BD50, serum dilution corresponding to 50% of maximum blocking activity) plotted against a-sACE2 for moderate and (D) severe COVID-19. Data for individual samples are shown; samples drawn after 15 days PSO are selected. Spearman correlation performed with a 95% confidence interval. (E) ED50 of anti-RBD IgG plotted against blocking of ACE2-binding (BD50). (F) ACE2 competition, (G) anti-RBD IgG, and (H) anti-nucleocapsid IgG confirmed for two sample groups with high (gray, N = 12) versus low (black line, N = 5) RBD titers. Positive and negative controls in blue and red, respectively. (I) Structural depiction of the RBD bound to CC12.1 and P2B-2F6. PDB: 6XDG , 7BWJ , and 6XC2 . (J) RBD binding of recombinant antibodies in competition with class 1 nAb CC12.1 and class 2 nAb P2B-2F6. (K) Localization of class 1 and 2 abrogating RBD mutations F456A and E484K. ACE2 footprint shown in blue. (L) RBD high versus low binding sera cleared by a pull-down with RBD WT, RBD-F456A, RBD-E484K, and MERS-CoV RBD as control. Remaining IgG binding to RBD and ACE2 competition is depicted in %.

Article Snippet: Anti-human ACE2 antibody 3215 , ProSci Incorporated , #3215.

Techniques: Binding Assay, Activity Assay, Sampling, MANN-WHITNEY, Whisker Assay, Blocking Assay, Recombinant, Control

Journal: iScience

Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

doi: 10.1016/j.isci.2024.109330

Figure Lengend Snippet: Soluble ACE2 interferes with the germinal center reaction in silico (A) Scheme depicting the germinal center (GC) response: GC reaction starts with an influx of low-affinity seeder cells. These cells are in a pro-apoptotic state and must acquire survival signals by antigen acquisition and T follicular helper cell (Tfh cell) signaling. Ag binding probability (P Ag ) is proportional to the mutational distance of the BCR to the Ag (MutDist, see and ). The Tfh cells preferentially provide signal to B cells that acquire larger amounts of antigen. Some of the selected B cells exit the GC and become output cells, whereas the rest recycle back and proliferate with mutations, resulting in daughter cells of higher affinity. These new cells again compete for survival signals, resulting in progressive B cell affinity increase. Serum sACE2 and the antibodies produced by output B cells can feedback to the GC by making antigen acquisition harder (mechanisms in B and C). (B) Epitope masking mechanism (scenario A): sACE2 and antibodies can bind to the antigen and mask it, thus lowering the amount of antigen available for B cells. (C) Epitope masking and mean field Ab-B cell competition mechanism (scenario B): BCR probability of binding the unmasked Ag is reduced depending on the average affinity of sACE2 and endogenous Abs (ACE2/Ab affinity). (D–K) Simulation results for different sACE2 concentrations (0, 1, 10, and 50 nM constant concentration in D–G; 0, 0.05, 0.23 nM constant concentration and 0.05–0.23 nM linear increase in H–K): IP (D, H) and GC size (E, I) with scenario A; IP (F, J) and GC size (G, K) with mean field Ab-B cell competition. (L–S) Simulation results for different sACE2 affinities (0.475, 1.9, and 3.8 nM in L–O; 5, 25, 125 nM in P–S): IP (L, P) and GC size (M, Q) with epitope masking only; IP (N, R) and GC size (O, S) with scenario B. Mean (continuous lines) and standard deviation (shaded area) of simulations for a total of 20 simulated GCs are shown. Schemes (A–C) are created with BioRender.

Article Snippet: Anti-human ACE2 antibody 3215 , ProSci Incorporated , #3215.

Techniques: In Silico, Binding Assay, Produced, Concentration Assay, Standard Deviation

Journal: iScience

Article Title: Soluble ACE2 correlates with severe COVID-19 and can impair antibody responses

doi: 10.1016/j.isci.2024.109330

Figure Lengend Snippet:

Article Snippet: Anti-human ACE2 antibody 3215 , ProSci Incorporated , #3215.

Techniques: Recombinant, Magnetic Beads, Software, In Silico

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 1 | High ACE2 expression was linked to increased VM and better prognosis in NSCLC. (A) Typical image of ACE2, VE-cadherin, EphA2 protein expression and CD34/PAS double staining in TMA tissues. Case B1 had massive CD34−/PAS+ VM (yellow arrows) lined by ACE2, VE-cadherin and EphA2 high expressing tumor cells. Case G1 had abundant CD34+/PAS−MVs (black arrows) with ACE2, VE-cadherin and EphA2 low expressing tumor cells. (B) Kaplan-Meier analysis of OS in NSCLC patients with ACE2 low or high expression. P = 0.044.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Expressing, Double Staining

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 2 | ACE2-induced better outcome in NSCLC patients might be attributed to less vessels and more VM formation. (A, C, E, G) Typical tissue images of each group stained with ACE2 or CD34/PAS. Yellow arrows: CD34−/PAS+ VMs; black arrows: CD34+/PAS−MV. (B, D, F, H) Kaplan–Meier analysis of OS in each group.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Staining

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 3 | Human ACE2 was stably overexpressed in A549-ACE2-OE cells. (A) Schematic representation of pLenti6.3-MCS/V5 DEST. (B) pLenti6.3-ACE2 expression vector was detected by PCR. (C) Fluorescence of EGFP in A549-ACE2-OE cells (left) and parental cells (right) was determined by fluorescence microscopy. (D) RT-PCR experiment of ACE2 mRNA level in A549-ACE2-OE cells and control cells, Mean ± SD, n = 3, *p < 0.05. (E) Western blot analysis of ACE2 expression level in A549-ACE2-OE cells and parental cells. (F) Quantification of ACE2 expression level in A549-ACE2-OE cells and parental cells. Mean ± SD, n = 3, ***p < 0.001.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Stable Transfection, Expressing, Plasmid Preparation, Fluorescence, Microscopy, Reverse Transcription Polymerase Chain Reaction, Control, Western Blot

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 4 | Tube formation ability of A549 cells was improved with ACE inhibitory state. (A) Morphologies of a panel of A549-ACE2-OE cells, A549-NC cells, and A549-NC cells treated with ACEI (1, 5, and 10 nM/L) were shown as sheet-like and thread-like cell types in 2D culture, which were outlined partly with yellow lines. Representative images were shown above. Upper: white light; lower: fluorescence. (B) Quantification of sheet-like or thread-like cells and pebble-like cells in three groups, representatively, Mean ± SD, n = 3, **p < 0.01. (C) Images of both above cell lines grown in 3D Matrix gel. A 10 nM/L ACEI dilution was performed. Representative images were shown above. Yellow arrows point out the free cancer cells escaping from tube wall and isolated segments. Upper: white light; lower: fluorescence. (D, E) Images of 3D culture were applied to determine average number of nodes, branches, isolated segments, meshes and mean mesh area in those groups, per field, Mean ± SD, n = 3, **p < 0.01, *p < 0.05. ns, no significance.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Isolation

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 5 | VM formation was increased, and vasculature was lessened due to inhibition of RAS in vivo. (A) Growth curve of allograft tumors of A549-ACE2-OE cells, A549-NC cells with or without ACEI treatment, Mean ± SD, n = 3, *p < 0.05. ns, no significance. (B) Weight of resected tumors, Mean ± SD, n = 3, **p < 0.01, *p < 0.05. (C) Continuous sections of allograft tumor tissues stained with PAS, CD34, VE-cadherin, or EphA2 immunohistochemical stain. Black arrow points out a typical MV (CD34+/PAS−); yellow arrows point out typical VM (CD34−/PAS+). (D) Quantification of MV and VM in different groups, Mean ± SD, n = 3, per field, ***p < 0.001, **p < 0.01. (E) Quantification of VE-cadherin and EphA2 mean optical density in three groups, Mean ± SD, n = 3, ***p < 0.001, **p < 0.01.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Inhibition, In Vivo, Staining, Immunohistochemical staining

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 6 | VE-cadherin and EphA2 expression was upregulated in A549 cells and NSCLC tissues with impaired local RAS status. (A, B) RT-PCR experiment of VE-cadherin and EphA2 mRNA level in A549-ACE2-OE cells and control cells, Mean ± SD, n = 3, ***p < 0.001. (C–E) Western blot analysis and quantification of VE- cadherin and EphA2 expression level in A549-ACE2-OE cells and control cells, Mean ± SD, n = 3, ***p < 0.001. (F, G) Linear regressions of VM number and VE- cadherin (P < 0.0001) or EphA2 (P = 0.0108) score in TMA. (H) Typical tissue images of both groups stained with VE-cadherin, ACE2 or CD34/PAS. Case F13 with ACE2 low status was provided with rambling VM covered by tumor cells which only expressed VE-cadherin in nuclei; case D6 with ACE2 high status had ordered VM lined by tumor cells expressing VE-cadherin in both nuclei and cytomembranes. Red arrow: VE-cadherin membrane expression.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Control, Western Blot, Staining, Membrane

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 7 | PI3K/AKT, p38MAPK, and HIF1-a were inactivated, and Nodal/Notch4 pathway was activated in A549-ACE2-OE cell model. (A–E) Western blot analysis and quantification of AKT, p-AKT, p38, and p-p38 expression level in A549-ACE2-OE cells and negative control, Mean ± SD, n = 3, ***p < 0.001, **p < 0.01. (F, G) Immunoflurescence assay and quantification of HIF1-a mean optical density in A549-ACE2-OE cells and negative control, Mean ± SD, n = 4, *p < 0.05. (H, I) Western blot analysis and quantification of Nodal and Notch4 expression level in A549-ACE2-OE cells and negative control, Mean ± SD, n = 3, ***p < 0.001, **p < 0.01.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Western Blot, Expressing, Negative Control

Journal: Cell Biology International

Article Title: Study of frequency and inheritance model of ACE1 I/D and ACE2 rs2285666 polymorphisms in COVID‐19 patients with varying severity of lung involvement and its effect on serum cytokines levels

doi: 10.1002/cbin.11977

Figure Lengend Snippet: Primer sequences, restriction enzymes, and amplified sequences for detection of ACE1 and ACE2 polymorphisms

Article Snippet: COVID‐19 and other SARS viruses typically infect cells by binding their glycoprotein receptors to the ACE‐2 receptor (Cristiani et al., ; Matheson & Lehner, ).

Techniques: Amplification

Journal: Cell Biology International

Article Title: Study of frequency and inheritance model of ACE1 I/D and ACE2 rs2285666 polymorphisms in COVID‐19 patients with varying severity of lung involvement and its effect on serum cytokines levels

doi: 10.1002/cbin.11977

Figure Lengend Snippet: PCR conditions for amplification of ACE1 and ACE2 sequences

Article Snippet: COVID‐19 and other SARS viruses typically infect cells by binding their glycoprotein receptors to the ACE‐2 receptor (Cristiani et al., ; Matheson & Lehner, ).

Techniques: Amplification

Journal: Cell Biology International

Article Title: Study of frequency and inheritance model of ACE1 I/D and ACE2 rs2285666 polymorphisms in COVID‐19 patients with varying severity of lung involvement and its effect on serum cytokines levels

doi: 10.1002/cbin.11977

Figure Lengend Snippet: Haplotype analysis of ACE1 and ACE2 polymorphisms in COVID‐19 hospitalized patients

Article Snippet: COVID‐19 and other SARS viruses typically infect cells by binding their glycoprotein receptors to the ACE‐2 receptor (Cristiani et al., ; Matheson & Lehner, ).

Techniques:

Journal: Cell Biology International

Article Title: Study of frequency and inheritance model of ACE1 I/D and ACE2 rs2285666 polymorphisms in COVID‐19 patients with varying severity of lung involvement and its effect on serum cytokines levels

doi: 10.1002/cbin.11977

Figure Lengend Snippet: Correlation analysis of the ACE1 I/D and ACE2 rs2285666 genotypes with clinical variables. (a) ACE1 I/I correlation with clinical variables. (b) ACE1 I/D correlation with clinical variables. (c) ACE1 D/D correlation with clinical variables. (d) ACE2 rs2285666 C/C correlation with clinical variables. (e) ACE2 rs2285666 C/T correlation with clinical variables. The numbers at the top of each cell represent the Pearson r value and the numbers at the bottom of the cells in parentheses represent the p value for the Pearson correlation test. The colors of the table cells show the degree of r correlation value between the studied variables. ACE, angiotensin‐converting enzyme; IL, interleukin; NLR, neutrophil‐to‐lymphocyte ratio.

Article Snippet: COVID‐19 and other SARS viruses typically infect cells by binding their glycoprotein receptors to the ACE‐2 receptor (Cristiani et al., ; Matheson & Lehner, ).

Techniques:

Journal: Viruses

Article Title: ACE2-Decoy-Conjugated PLGA-PEG Nanoparticles Loaded with Nafamostat for Potent Antiviral Activity

doi: 10.3390/v17091167

Figure Lengend Snippet: Schematic diagram of nafamostat-loaded ACE2 decoy-modified nanoparticles.

Article Snippet: Notable examples include the rationally designed ACE2 decoys CTC-445.2d (IC 50 < 5 nM) and peptide mimetics SI5α (IC 50 = 1.59 μM), both of which show potent antiviral activity across multiple cell models [ , ].

Techniques: Modification

Journal: Viruses

Article Title: ACE2-Decoy-Conjugated PLGA-PEG Nanoparticles Loaded with Nafamostat for Potent Antiviral Activity

doi: 10.3390/v17091167

Figure Lengend Snippet: The concentration-dependent cytotoxicity of NM, Pro, NM-PP NPs, and NM-PP-Pro NPs in 293T cell ( A ) and 293T-ACE2 cell ( B ). The cells’ viability was determined by means of the CCK-8 assay and is expressed as the ratio of non-treated cells.

Article Snippet: Notable examples include the rationally designed ACE2 decoys CTC-445.2d (IC 50 < 5 nM) and peptide mimetics SI5α (IC 50 = 1.59 μM), both of which show potent antiviral activity across multiple cell models [ , ].

Techniques: Concentration Assay, CCK-8 Assay

Journal: Viruses

Article Title: ACE2-Decoy-Conjugated PLGA-PEG Nanoparticles Loaded with Nafamostat for Potent Antiviral Activity

doi: 10.3390/v17091167

Figure Lengend Snippet: Visualization of 6-Coumarin-labeled (green) NM-PP-Pro NPs in 293T-ACE2 and RAW 264.7 cells (blue) via fluorescence microscope.

Article Snippet: Notable examples include the rationally designed ACE2 decoys CTC-445.2d (IC 50 < 5 nM) and peptide mimetics SI5α (IC 50 = 1.59 μM), both of which show potent antiviral activity across multiple cell models [ , ].

Techniques: Labeling, Fluorescence, Microscopy