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InvivoGen hek bluetm null1 v cells
Hek Bluetm Null1 V Cells, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 39 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/hek+bluetm+cells/HEK-Blue+Null1-v+Cells/10__3390_slash_biom16060795-129-3-6
Average 94 stars, based on 39 article reviews

hek bluetm null1 v cells - by Bioz Stars, 2026-09

94/100 stars

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Stable Transfection:

Article Title: Three semi-synthetic approaches to a set of curdlan sulfate polysaccharides with different sulfation patterns
Article Snippet: .. HEK-BlueTM cells, human embryonic kidney cell line HEK293 stably co-transfected with secreted embryonic alkaline phosphatase (SEAP), and the human (h) TLR2 and TLR4 were cultured in DMEM with 10% FBS (v/v) and selective antibiotics as required in the handling procedure (InvivoGen) in a humidified atmosphere (5% CO 2 , 95% air) at 37°C. ..

Cell Culture:

Article Title: Cancer cell genetics shaping of the tumor microenvironment reveals myeloid cell-centric exploitable vulnerabilities in hepatocellular carcinoma.
Article Snippet: FBS-12A), 1% penicillin/streptomycin (Roche) and 1% insulin-Transferrin-Selenium (ITS) (Gibco) (referred to as complete F12 medium)114. .. HEK-BlueTM cells (Invivogen cat. code hkb-il1r) were cultured in completemedium supplementedwith 100 μg/mLNormocin according to the manufacturer’s instructions. .. All cell lines were cultured at 37 °C and 5% CO2 and routinely tested for mycoplasma contamination using a MycoAlert® mycoplasma detection kit (Lonza, cat: LT07-218).

Activation Assay:

Article Title: The influence of calcium on pectin's impact on TLR2 signalling.
Article Snippet: .. To study whether pectins can activate or inhibit TLR2, activation or inhibition assays were performed with pectins using HEK-BlueTM cells expressing human TLR2 (Invivogen). ..

Inhibition:

Expressing:

Control:

Article Title: A positive feedback loop driven by fibronectin and IL-1β sustains the inflammatory microenvironment in breast cancer.
Article Snippet: .. Then, the supernatants were collected and applied (20 μL) onto HEK-BlueTM cells (5 × 104 cells/180 μL; Null2, InvivoGen, USA), which carry a secreted embryonic alkaline phosphatase (SEAP) reporter gene under the control of NF-κB, for 16 h in HEK-BlueTM Detection medium (InvivoGen). .. SEAP activity was evaluated at 650 nm (SpectraMax Plus, Molecular Devices, USA).

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( a , e and h ) HEK-TLR7 and HEK-TLR8 cells were pre-treated ∼30 min with 125 nM (TLR7) and 5 μM (TLR8) of the indicated oligos prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to GUC-v1+R848 [ a (TLR7)], GUC+R848 [ a (TLR8), and e ] and R848 [ h ] condition; a [TLR7 and TLR8]: P<0.0001 ; e [TLR7]: P<0.0001 and [TLR8]: P=0.0005 ; h [TLR7 and TLR8]: P<0.0001 ). ( c , g and j ) HEK-TLR7 cells were pre-treated ∼30 min with 50 nM of the indicated oligos prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to GUC+R848 ( c and g ) and GUC-v1+R848 ( j ) condition; c , g and j : P<0.0001 ). ( d ) HEK-TLR7 cells were pre-treated ∼30 min with different doses (1000 nM, 500 nM, 250 nM, 125 nM and 62.5 nM) of the indicated oligos and Enpatoran (100 nM, 50 nM, 25 nM, 12.5 nM and 6.25 nM) prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 only condition).

Journal: bioRxiv

Article Title: Defining the Immunomodulatory Determinants of 3-mer Oligonucleotides on TLR7 and TLR8 sensing

doi: 10.64898/2026.04.29.720527

Figure Lengend Snippet: ( a , e and h ) HEK-TLR7 and HEK-TLR8 cells were pre-treated ∼30 min with 125 nM (TLR7) and 5 μM (TLR8) of the indicated oligos prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to GUC-v1+R848 [ a (TLR7)], GUC+R848 [ a (TLR8), and e ] and R848 [ h ] condition; a [TLR7 and TLR8]: P<0.0001 ; e [TLR7]: P<0.0001 and [TLR8]: P=0.0005 ; h [TLR7 and TLR8]: P<0.0001 ). ( c , g and j ) HEK-TLR7 cells were pre-treated ∼30 min with 50 nM of the indicated oligos prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to GUC+R848 ( c and g ) and GUC-v1+R848 ( j ) condition; c , g and j : P<0.0001 ). ( d ) HEK-TLR7 cells were pre-treated ∼30 min with different doses (1000 nM, 500 nM, 250 nM, 125 nM and 62.5 nM) of the indicated oligos and Enpatoran (100 nM, 50 nM, 25 nM, 12.5 nM and 6.25 nM) prior to overnight stimulation with 1 μg/ml of R848 followed by luciferase assay. Data are mean of n=3 independent experiments. Data were background-corrected using the non-treated (NT) condition and are shown as relative expression to R848 only (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 only condition).

Article Snippet: HEK-BlueTM TLR7 (Invivogen, hkb-htlr7v2) reporter cells were cultured according to the manufacturer’s instructions and plated in complete DMEM prior to treatment.

Techniques: Luciferase, Expressing

( a-c ) Surface plasmon resonance (SPR) analyses of recombinant wild type human TLR8 ( a , b ), wild type mmTLR7 ( c ), mutant TLR8 (F495S) or mutant mmTLR7 (F507S) with the indicated concentrations of indicated 3-mers. Data shown are representative of 3-4 independent analyses (Supplementary Table S3). ( d, e ) Cryo-EM structure of the TLR7/GUC-v16 complex and crystal structure of the TLR8/GUC-v16 complex. Two TLR7 or TLR8 protomers and GUC-v16 are shown in cartoon and sphere representations, respectively. ( f, g ) Close-up views of the GUC-v16 (mImUmC PS ) recognition at the antagonistic sites of TLR7 and TLR8. Residues within 4.5 Å from GUC-v16 are shown in stick representations. Sticks are colored by atoms, with the N, O, P and S atoms colored by blue, red, orange and yellow, respectively. Yellow dashed lines indicate hydrogen bonds (cutoff distance < 3.5 Å). ( h ) Structural alignment of TLR7/GUC-v16 and TLR8/GUC-v16 complexes. Structural alignment was performed using the Matchmaker tool in ChimeraX.

Journal: bioRxiv

Article Title: Defining the Immunomodulatory Determinants of 3-mer Oligonucleotides on TLR7 and TLR8 sensing

doi: 10.64898/2026.04.29.720527

Figure Lengend Snippet: ( a-c ) Surface plasmon resonance (SPR) analyses of recombinant wild type human TLR8 ( a , b ), wild type mmTLR7 ( c ), mutant TLR8 (F495S) or mutant mmTLR7 (F507S) with the indicated concentrations of indicated 3-mers. Data shown are representative of 3-4 independent analyses (Supplementary Table S3). ( d, e ) Cryo-EM structure of the TLR7/GUC-v16 complex and crystal structure of the TLR8/GUC-v16 complex. Two TLR7 or TLR8 protomers and GUC-v16 are shown in cartoon and sphere representations, respectively. ( f, g ) Close-up views of the GUC-v16 (mImUmC PS ) recognition at the antagonistic sites of TLR7 and TLR8. Residues within 4.5 Å from GUC-v16 are shown in stick representations. Sticks are colored by atoms, with the N, O, P and S atoms colored by blue, red, orange and yellow, respectively. Yellow dashed lines indicate hydrogen bonds (cutoff distance < 3.5 Å). ( h ) Structural alignment of TLR7/GUC-v16 and TLR8/GUC-v16 complexes. Structural alignment was performed using the Matchmaker tool in ChimeraX.

Article Snippet: HEK-BlueTM TLR7 (Invivogen, hkb-htlr7v2) reporter cells were cultured according to the manufacturer’s instructions and plated in complete DMEM prior to treatment.

Techniques: SPR Assay, Recombinant, Mutagenesis, Cryo-EM Sample Prep

( a ) Bone-marrow-derived macrophages (BMDMs) from Tlr7 Y264H mice were treated for 24 h with 1 μM of BMS905 and 5 μM of GUC-v16 oligo prior to RNA purification for RNA-sequencing or RT-qPCR analyses. RT-qPCR analyses of Fpr1, Slc13a3, Cd300e, Itgal, Nfkbiz, Slamf9, Clec4a2 and Clec4a1 reported to 18S in RNA lysates from primary BMDMs from 3 independent Tlr7 Y264H mice. Data are shown relative to non-treated (NT) mice (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to NT Tlr7 Y264H condition). ( b ) WT C57/BL6 mice were injected i.v. with 200 μg of GUC-v16 conjugated with in vivo -jetPEI® or vehicle (glucose solution) for 1 h prior to i.p. injection of 25 μg R848 for 2 h before collection of spleens. RT-qPCR analyses of Fpr1, Fpr2, Marco, Nfkbiz and Tnf reported to Gapdh , from spleen lysates; data are shown relative to non-treated (NT) mice (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 mice). Each dot represents an individual mouse with bars showing the mean of n=5 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 group). ( c ) Aldara cream was applied topically to the back of WT C57/BL6 mice directly following, or not, application of 100 μl of highly pure 2.5% GUC-v16 cream oligonucleotide (>99.4%). After four days, mice were humanely euthanised and back skin collected, and lysed for RNA purification. RT-qPCR analyses of indicated genes reported to that of 18S expression, relative to NT mice. Data are representative of 2 independent experiments. Mean of n=3 NT and n=8 Aldara/Aldara+GUC-v16 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to Aldara group). ( d-f ) Wild type C57BL/6J mice were treated i.t. with 2.5 μg of naked GUC-v16 in water for 1 h prior to. i.t. injection of 50 μg of R848. BALF ( d, f ) were harvested 7 h post R848 injection and analysed by cytospin differential cell counting for total cell counts ( d ) and using an MSD multiplex assay for cytokine quantification ( f ). Cytokine levels in plasma were also quantified using an MSD multiplex assay ( e ). Data shown are from 1 experiment, representative of n=2 independent experiments. Mean of n=5 NT and n=7 R848/R848+GUC-v16 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to NT [d] or R848 [ e,f ] group). Whole blood from 4 ( g ) or 1 ( h ) healthy controls or patients with UNC93B1 E92G mutation ( h ) was pre-treated with indicated 3-mer concentration for 30 min prior to stimulation with indicated amount of R837 or 50ng/ml TL8-506 for 24 h prior to cytokine bead analyses. ( g ) For each control, cytokine levels were averaged for each technical replicate (6/sample), background corrected to unstimulated samples only, and reported to cytokine levels from stimulation only controls. Heat maps were generated using scale from 0-1 (see methods), were 1 is the cytokine level of the agonist only control. ( g-h ) Data shown are from a minimum of two independent experiments – conducted on two independent days. ( i ) HEK-TLR7 cells were pre-treated with indicated concentration of oligo for 1 h prior to overnight stimulation with 10% of synovial fluid from RA patient. SEAP absorbances were background-corrected using the non-treated condition, and are shown as relative expression to the synovial fluid only control; Neg. is a non-oligo condition used as control. Data shown are averaged from synovial fluid stimulations from n=8 patients (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to Neg condition).

Journal: bioRxiv

Article Title: Defining the Immunomodulatory Determinants of 3-mer Oligonucleotides on TLR7 and TLR8 sensing

doi: 10.64898/2026.04.29.720527

Figure Lengend Snippet: ( a ) Bone-marrow-derived macrophages (BMDMs) from Tlr7 Y264H mice were treated for 24 h with 1 μM of BMS905 and 5 μM of GUC-v16 oligo prior to RNA purification for RNA-sequencing or RT-qPCR analyses. RT-qPCR analyses of Fpr1, Slc13a3, Cd300e, Itgal, Nfkbiz, Slamf9, Clec4a2 and Clec4a1 reported to 18S in RNA lysates from primary BMDMs from 3 independent Tlr7 Y264H mice. Data are shown relative to non-treated (NT) mice (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to NT Tlr7 Y264H condition). ( b ) WT C57/BL6 mice were injected i.v. with 200 μg of GUC-v16 conjugated with in vivo -jetPEI® or vehicle (glucose solution) for 1 h prior to i.p. injection of 25 μg R848 for 2 h before collection of spleens. RT-qPCR analyses of Fpr1, Fpr2, Marco, Nfkbiz and Tnf reported to Gapdh , from spleen lysates; data are shown relative to non-treated (NT) mice (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 mice). Each dot represents an individual mouse with bars showing the mean of n=5 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to R848 group). ( c ) Aldara cream was applied topically to the back of WT C57/BL6 mice directly following, or not, application of 100 μl of highly pure 2.5% GUC-v16 cream oligonucleotide (>99.4%). After four days, mice were humanely euthanised and back skin collected, and lysed for RNA purification. RT-qPCR analyses of indicated genes reported to that of 18S expression, relative to NT mice. Data are representative of 2 independent experiments. Mean of n=3 NT and n=8 Aldara/Aldara+GUC-v16 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to Aldara group). ( d-f ) Wild type C57BL/6J mice were treated i.t. with 2.5 μg of naked GUC-v16 in water for 1 h prior to. i.t. injection of 50 μg of R848. BALF ( d, f ) were harvested 7 h post R848 injection and analysed by cytospin differential cell counting for total cell counts ( d ) and using an MSD multiplex assay for cytokine quantification ( f ). Cytokine levels in plasma were also quantified using an MSD multiplex assay ( e ). Data shown are from 1 experiment, representative of n=2 independent experiments. Mean of n=5 NT and n=7 R848/R848+GUC-v16 mice/group is shown (± s.e.m. and one-way ANOVA with uncorrected Fisher’s LSD tests shown compared to NT [d] or R848 [ e,f ] group). Whole blood from 4 ( g ) or 1 ( h ) healthy controls or patients with UNC93B1 E92G mutation ( h ) was pre-treated with indicated 3-mer concentration for 30 min prior to stimulation with indicated amount of R837 or 50ng/ml TL8-506 for 24 h prior to cytokine bead analyses. ( g ) For each control, cytokine levels were averaged for each technical replicate (6/sample), background corrected to unstimulated samples only, and reported to cytokine levels from stimulation only controls. Heat maps were generated using scale from 0-1 (see methods), were 1 is the cytokine level of the agonist only control. ( g-h ) Data shown are from a minimum of two independent experiments – conducted on two independent days. ( i ) HEK-TLR7 cells were pre-treated with indicated concentration of oligo for 1 h prior to overnight stimulation with 10% of synovial fluid from RA patient. SEAP absorbances were background-corrected using the non-treated condition, and are shown as relative expression to the synovial fluid only control; Neg. is a non-oligo condition used as control. Data shown are averaged from synovial fluid stimulations from n=8 patients (± s.e.m. and two-way ANOVA with uncorrected Fisher’s LSD tests shown compared to Neg condition).

Article Snippet: HEK-BlueTM TLR7 (Invivogen, hkb-htlr7v2) reporter cells were cultured according to the manufacturer’s instructions and plated in complete DMEM prior to treatment.

Techniques: Derivative Assay, Purification, RNA Sequencing, Quantitative RT-PCR, Injection, In Vivo, Cream, Expressing, Cell Counting, Multiplex Assay, Clinical Proteomics, Mutagenesis, Concentration Assay, Control, Generated

a , Schematic overview of SPID-based rapid antibody library production and antibody characterization. b , Binding curves for HER2-eGFP to trastuzumab scFab used for K D fitting. c , Comparison of K D values for the trastuzumab scFab-HER2 interaction obtained by single-reaction estimates and curve fitting (two-sided one-sample t-test, p =0.30). d , Correlation of K D values measured using SPID and previously reported values of original antibodies. A total of 36 distinct antibody sequence-based scFabs were analyzed to assess the correlation between their measured affinities and the reported IgG values. e , Deep mutational scanning (DMS) of K D changes in trastuzumab scFab-HER2 interactions from single-residue variations in CDRs (HCDR2, HCDR3, and LCDR2) and the framework region 3 (F3). f , Affinity DMS heatmap of trastuzumab IgG HCDR3 variants corresponding to ( e ). g, Comparison of K D values measured via SPID between trastuzumab scFab and IgG single-residue variants. h , DMS of expression metrics for adalimumab scFab single-residue variants. i , Correlation between SPID-measured expression metrics and productivity from large-scale (up to 10 liters) cultures of anti-TNF-α or anti-GIPR antibodies in HEK293F cells. j , DMS of adalimumab scFab-TNF-α binding after 60 °C heat treatment (Ab: antibody, Ag: antigen). k, Changes of TNF-α binding for adalimumab IgG as a function of heat treatment temperature ( T ₘ: Melting temperature). l, Correlation between T ₘ values determined by SPID and the Differential Scanning Fluorimetry (DSF) method.

Journal: bioRxiv

Article Title: Landscape-scale navigation unlocks antibody CDR structural logic for AI-guided rescue and therapeutic optimization

doi: 10.64898/2026.04.21.719857

Figure Lengend Snippet: a , Schematic overview of SPID-based rapid antibody library production and antibody characterization. b , Binding curves for HER2-eGFP to trastuzumab scFab used for K D fitting. c , Comparison of K D values for the trastuzumab scFab-HER2 interaction obtained by single-reaction estimates and curve fitting (two-sided one-sample t-test, p =0.30). d , Correlation of K D values measured using SPID and previously reported values of original antibodies. A total of 36 distinct antibody sequence-based scFabs were analyzed to assess the correlation between their measured affinities and the reported IgG values. e , Deep mutational scanning (DMS) of K D changes in trastuzumab scFab-HER2 interactions from single-residue variations in CDRs (HCDR2, HCDR3, and LCDR2) and the framework region 3 (F3). f , Affinity DMS heatmap of trastuzumab IgG HCDR3 variants corresponding to ( e ). g, Comparison of K D values measured via SPID between trastuzumab scFab and IgG single-residue variants. h , DMS of expression metrics for adalimumab scFab single-residue variants. i , Correlation between SPID-measured expression metrics and productivity from large-scale (up to 10 liters) cultures of anti-TNF-α or anti-GIPR antibodies in HEK293F cells. j , DMS of adalimumab scFab-TNF-α binding after 60 °C heat treatment (Ab: antibody, Ag: antigen). k, Changes of TNF-α binding for adalimumab IgG as a function of heat treatment temperature ( T ₘ: Melting temperature). l, Correlation between T ₘ values determined by SPID and the Differential Scanning Fluorimetry (DSF) method.

Article Snippet: HEK-BlueTM TNF-α cells were purchased from InvivoGen.

Techniques: Binding Assay, Comparison, Sequencing, Residue, Expressing

a, Fluorescence distribution of single adalimumab–target complexes. Rightward fluorescence shifts per spot indicate preferential binding of adalimumab to trimeric TNF-α over the monomeric form (eGFP). b, Schematic of sequence vectorization, where each variant is encoded as a 27-dimensional physicochemical vector (hydrophobicity, volume, isoelectric point) before UMAP projection. c, Correlation between mutational steps and UMAP Euclidean distance, showing spatial expansion with increasing mutational load (Spearman’s ρ = 0.415). d, Heatmap correlating mutation counts between each sequence and its UMAP neighbors, demonstrating high local topographical consistency (90.3%). e–j, Topographical distribution and mutational enrichment across three major clusters: (e and f) peak cluster, (g and h) rugged interface, and (i and j) broad valley. Histograms show fold enrichment of single mutations within each cluster. k, Bubble chart summarizing mutational enrichment across topographical groups, with bubble size indicating enrichment magnitude and color denoting significance (p-value). l, Fitness scatter plot (expression metric versus relative occupancy) color-coded by topographical assignment: peak cluster (red), rugged interface (brown), broad valley (blue), and others (gray).

Journal: bioRxiv

Article Title: Landscape-scale navigation unlocks antibody CDR structural logic for AI-guided rescue and therapeutic optimization

doi: 10.64898/2026.04.21.719857

Figure Lengend Snippet: a, Fluorescence distribution of single adalimumab–target complexes. Rightward fluorescence shifts per spot indicate preferential binding of adalimumab to trimeric TNF-α over the monomeric form (eGFP). b, Schematic of sequence vectorization, where each variant is encoded as a 27-dimensional physicochemical vector (hydrophobicity, volume, isoelectric point) before UMAP projection. c, Correlation between mutational steps and UMAP Euclidean distance, showing spatial expansion with increasing mutational load (Spearman’s ρ = 0.415). d, Heatmap correlating mutation counts between each sequence and its UMAP neighbors, demonstrating high local topographical consistency (90.3%). e–j, Topographical distribution and mutational enrichment across three major clusters: (e and f) peak cluster, (g and h) rugged interface, and (i and j) broad valley. Histograms show fold enrichment of single mutations within each cluster. k, Bubble chart summarizing mutational enrichment across topographical groups, with bubble size indicating enrichment magnitude and color denoting significance (p-value). l, Fitness scatter plot (expression metric versus relative occupancy) color-coded by topographical assignment: peak cluster (red), rugged interface (brown), broad valley (blue), and others (gray).

Article Snippet: HEK-BlueTM TNF-α cells were purchased from InvivoGen.

Techniques: Fluorescence, Binding Assay, Sequencing, Variant Assay, Plasmid Preparation, Mutagenesis, Expressing

a , HCDR2 and HCDR3 sequences of the parental adalimumab and the engineered variants. b-e, Comprehensive profiling of engineered adalimumab variants. ( b ) Volumetric productivity of parental adalimumab and clones 1207 and 1208, purified from 40 ml HEK293F cultures. ( c ) Correlation between SPID-measured expression metrics and productivity across large-scale (up to 10 liters) cultures of anti-TNF-α or anti-GIPR antibodies in HEK293F cells. Data points for clones 1207 and 1208, produced in 7L cultures, are explicitly highlighted. ( d ) Thermal stability assessment via melting curve analysis. ( e ) Dose-dependent binding curves with trimeric TNF-α with SPID. f, In vitro neutralization activity assessed using an NF-κB–responsive SEAP reporter assay. g, Concentration-response analysis and calculated IC ₅₀ values demonstrate the enhanced neutralizing potency of the engineered clones. h, Body weight change (%) of mice during the experiment, indicating no significant treatment-related toxicity. i, Detailed PASI score components (skin score (erythema and scaling) and thickness) plotted over the 7-day treatment period. j, Dose-response relationship for adalimumab, clone1207, and clone1208 based on PASI scores at day 7.

Journal: bioRxiv

Article Title: Landscape-scale navigation unlocks antibody CDR structural logic for AI-guided rescue and therapeutic optimization

doi: 10.64898/2026.04.21.719857

Figure Lengend Snippet: a , HCDR2 and HCDR3 sequences of the parental adalimumab and the engineered variants. b-e, Comprehensive profiling of engineered adalimumab variants. ( b ) Volumetric productivity of parental adalimumab and clones 1207 and 1208, purified from 40 ml HEK293F cultures. ( c ) Correlation between SPID-measured expression metrics and productivity across large-scale (up to 10 liters) cultures of anti-TNF-α or anti-GIPR antibodies in HEK293F cells. Data points for clones 1207 and 1208, produced in 7L cultures, are explicitly highlighted. ( d ) Thermal stability assessment via melting curve analysis. ( e ) Dose-dependent binding curves with trimeric TNF-α with SPID. f, In vitro neutralization activity assessed using an NF-κB–responsive SEAP reporter assay. g, Concentration-response analysis and calculated IC ₅₀ values demonstrate the enhanced neutralizing potency of the engineered clones. h, Body weight change (%) of mice during the experiment, indicating no significant treatment-related toxicity. i, Detailed PASI score components (skin score (erythema and scaling) and thickness) plotted over the 7-day treatment period. j, Dose-response relationship for adalimumab, clone1207, and clone1208 based on PASI scores at day 7.

Article Snippet: HEK-BlueTM TNF-α cells were purchased from InvivoGen.

Techniques: Clone Assay, Purification, Expressing, Produced, Binding Assay, In Vitro, Neutralization, Activity Assay, Reporter Assay, Concentration Assay

a, Functional inhibition of TNF-α signaling measured in an NF-κB responsive SEAP reporter assay using HEK293 cells. Concentration-response curves show improved neutralizing potency of engineered adalimumab variants clone1207 (IC 50 =15.3 pM) and clone1208 (IC 50 =26.2 pM) compared to Adalimumab (IC 50 =278.8 pM). b, Schematic of the imiquimod (IMQ)-induced psoriasis mouse model. c, Changes in daily Psoriasis Area and Severity Index (PASI) scores during treatment journey. d, Monitoring of body weight changes during treatment journey showing no overt toxicity. e, Representative macroscopic appearance of dorsal skin on day 7. f, Representative histological and immunohistochemical staining of dorsal skin lesions on day 7. The photographs show suppression of epidermal hyperplasia (H&E), reduced keratinocyte hyperproliferation (Ki67), and decreased inflammatory cytokine expression (IL-17A). The complete set of images for ( e ) and ( f ) is provided in Extended Data Fig. 10. g, Quantification of Ki67 + cells from tissue sections. h,i, Inflammatory cytokine levels within skin lesions: ( h ) IL-17A and ( i ) IL-6. j, Dose-response analysis of PASI scores at day 7 demonstrating dose-sparing efficacy of clones 1207 and 1208. k, Spleen index measured on day 7 as an indicator of systemic inflammation. l , Representative images of spleens collected on day 7. m , Comparison of residual Ab-Ag complex lifetimes between adalimumab variants and TNF-α using SPID.

Journal: bioRxiv

Article Title: Landscape-scale navigation unlocks antibody CDR structural logic for AI-guided rescue and therapeutic optimization

doi: 10.64898/2026.04.21.719857

Figure Lengend Snippet: a, Functional inhibition of TNF-α signaling measured in an NF-κB responsive SEAP reporter assay using HEK293 cells. Concentration-response curves show improved neutralizing potency of engineered adalimumab variants clone1207 (IC 50 =15.3 pM) and clone1208 (IC 50 =26.2 pM) compared to Adalimumab (IC 50 =278.8 pM). b, Schematic of the imiquimod (IMQ)-induced psoriasis mouse model. c, Changes in daily Psoriasis Area and Severity Index (PASI) scores during treatment journey. d, Monitoring of body weight changes during treatment journey showing no overt toxicity. e, Representative macroscopic appearance of dorsal skin on day 7. f, Representative histological and immunohistochemical staining of dorsal skin lesions on day 7. The photographs show suppression of epidermal hyperplasia (H&E), reduced keratinocyte hyperproliferation (Ki67), and decreased inflammatory cytokine expression (IL-17A). The complete set of images for ( e ) and ( f ) is provided in Extended Data Fig. 10. g, Quantification of Ki67 + cells from tissue sections. h,i, Inflammatory cytokine levels within skin lesions: ( h ) IL-17A and ( i ) IL-6. j, Dose-response analysis of PASI scores at day 7 demonstrating dose-sparing efficacy of clones 1207 and 1208. k, Spleen index measured on day 7 as an indicator of systemic inflammation. l , Representative images of spleens collected on day 7. m , Comparison of residual Ab-Ag complex lifetimes between adalimumab variants and TNF-α using SPID.

Article Snippet: HEK-BlueTM TNF-α cells were purchased from InvivoGen.

Techniques: Functional Assay, Inhibition, Reporter Assay, Concentration Assay, Immunohistochemical staining, Staining, Expressing, Clone Assay, Comparison

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hek bluetm null1 v cells (InvivoGen)

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