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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines <t>(A-431</t> and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.
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Image Search Results


In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines (A-431 and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.

Journal: Molecular Therapy Oncology

Article Title: KLS-3021: Innovative oncolytic virotherapy for the treatment of advanced primary and metastatic cutaneous squamous cell carcinoma

doi: 10.1016/j.omton.2026.201182

Figure Lengend Snippet: In vitro cytotoxicity and tumor-restricted replication analysis of KLS-3021 in cSCC cells (A) Schematic representation of KLS-3021 showing deletions of C11R , K3L , and J2R loci and insertions of therapeutic genes encoding PH-20, IL-12, and sPD1-Fc. (B) Cytotoxicity of KLS-3021 in human cSCC cell lines (A-431 and HSC-1) and normal human epidermal keratinocytes (NHEKs) was measured via CCK-8 assay at 72 h post-infection. (C) Viral replication in cSCC cell lines and NHEKs was determined via TCID 50 assay at 72 h post-infection. Data was represented as mean ± SEM of three independent experiments.

Article Snippet: Luciferase-labeled A-431 cells were cultured in DMEM (ATCC) supplemented with 10% FBS (Gibco), 1% penicillin-streptomycin (Sigma), and 8 μg/mL blasticidin (InvivoGen).

Techniques: In Vitro, CCK-8 Assay, Infection

Tumor growth analysis in orthotopic primary cSCC model following KLS-3021 treatment (A) Schematic of the experimental design for the orthotopic cSCC model established by intradermal implantation of A-431 cells. (B) Tumor growth curves of vehicle-treated and KLS-3021-treated mice (mean ± SEM, n = 6 per group; ∗∗∗ p < 0.001 by two-tailed t test). (C) Individual tumor growth curves for each mouse. (D) Body-weight changes during the observation period were represented (mean ± SEM). (E and F) Representative hematoxylin and eosin (H&E)-stained sections of tumors collected on days 3 (E) and 7 (F) post-treatment. Scale bars, 300 μm; enlarged views, 100 μm.

Journal: Molecular Therapy Oncology

Article Title: KLS-3021: Innovative oncolytic virotherapy for the treatment of advanced primary and metastatic cutaneous squamous cell carcinoma

doi: 10.1016/j.omton.2026.201182

Figure Lengend Snippet: Tumor growth analysis in orthotopic primary cSCC model following KLS-3021 treatment (A) Schematic of the experimental design for the orthotopic cSCC model established by intradermal implantation of A-431 cells. (B) Tumor growth curves of vehicle-treated and KLS-3021-treated mice (mean ± SEM, n = 6 per group; ∗∗∗ p < 0.001 by two-tailed t test). (C) Individual tumor growth curves for each mouse. (D) Body-weight changes during the observation period were represented (mean ± SEM). (E and F) Representative hematoxylin and eosin (H&E)-stained sections of tumors collected on days 3 (E) and 7 (F) post-treatment. Scale bars, 300 μm; enlarged views, 100 μm.

Article Snippet: Luciferase-labeled A-431 cells were cultured in DMEM (ATCC) supplemented with 10% FBS (Gibco), 1% penicillin-streptomycin (Sigma), and 8 μg/mL blasticidin (InvivoGen).

Techniques: Two Tailed Test, Staining

Bioluminescence imaging and tissue analysis in metastatic cSCC model following KLS-3021 treatment (A) Schematic of the experimental design for the orthotopic metastatic cSCC model established by intradermal implantation of luciferase-labeled A-431 cells into the footpad. (B) Longitudinal quantification of total photon flux from the primary tumor and popliteal lymph node (PLN) at each time point post-treatment ( n = 5 per group; ∗∗∗ p < 0.001 by two-tailed t test). (C) Representative IVIS bioluminescence images showing signals from primary and nodal tumors in vehicle- and KLS-3021-treated mice at indicated time points. (D and E) Primary tumor weights (D) and PLN weights (E) measured on day 3 ( n = 5 per group; ∗ p < 0.05 by two-tailed t test) and day 28 ( n = 10 per group; ∗ p < 0.05, ∗∗∗ p < 0.001 by two-tailed t test) post-treatment. All data were represented as mean ± SEM.

Journal: Molecular Therapy Oncology

Article Title: KLS-3021: Innovative oncolytic virotherapy for the treatment of advanced primary and metastatic cutaneous squamous cell carcinoma

doi: 10.1016/j.omton.2026.201182

Figure Lengend Snippet: Bioluminescence imaging and tissue analysis in metastatic cSCC model following KLS-3021 treatment (A) Schematic of the experimental design for the orthotopic metastatic cSCC model established by intradermal implantation of luciferase-labeled A-431 cells into the footpad. (B) Longitudinal quantification of total photon flux from the primary tumor and popliteal lymph node (PLN) at each time point post-treatment ( n = 5 per group; ∗∗∗ p < 0.001 by two-tailed t test). (C) Representative IVIS bioluminescence images showing signals from primary and nodal tumors in vehicle- and KLS-3021-treated mice at indicated time points. (D and E) Primary tumor weights (D) and PLN weights (E) measured on day 3 ( n = 5 per group; ∗ p < 0.05 by two-tailed t test) and day 28 ( n = 10 per group; ∗ p < 0.05, ∗∗∗ p < 0.001 by two-tailed t test) post-treatment. All data were represented as mean ± SEM.

Article Snippet: Luciferase-labeled A-431 cells were cultured in DMEM (ATCC) supplemented with 10% FBS (Gibco), 1% penicillin-streptomycin (Sigma), and 8 μg/mL blasticidin (InvivoGen).

Techniques: Imaging, Luciferase, Labeling, Two Tailed Test