Fig. 8: Clinical implications of PAMT-001 in cancers with treatment resistance and AML patients, particularly those with NPM1 mutations.

A CCK-8 assay of PAMT-001-treated primary AML (n = 28) and normal mononuclear (n = 8) cells. LD₅₀ values were calculated through [inhibitor] vs. normalized response—Variable slope in Prism 8. P-values were calculated using the extra sum of squares F-test (mean ± SD). B CCK-8 assay of PAMT-001- or cytarabine-treated KG1α cells. LD₅₀ values were calculated through [inhibitor] vs. normalized response—Variable slope in Prism 8. P-values were calculated using a two-sided t-test (mean ± SD, n = 4). C MTT assay of gefitinib- or PAMT-001-treated PC-9 cells (lung cancer). P-values were calculated using a two-sided t-test (mean ± SD, n = 6). D Correlation analysis of LD₅₀ value for PAMT-001 and AML patient characteristics using Pearson correlation coefficients. E LD₅₀ value for PAMT-001 according to the gender of the patient with AML (left), risk stratification based on NCCN guidelines (middle), and responses against standard treatment (Idarubicin and cytarabine) (right). P-value was calculated using a two-sided t-test (gender and response against standard treatments) or one-way ANOVA for multiple comparisons (risk stratification). F Simple logistic regression between the mutation profiles of patients with AML and LD₅₀ of PAMT-001. G Primary AML cells with NPM1 mutation showed more sensitivity to PAMT-001 than cells with normal NPM1 status. P-value was calculated using a two-sided t-test (mean ± SD). H Gene set enrichment analysis against Hallmark oxidative phosphorylation. Genes were ranked based on fold changes between normal and mutant NPM1 status in TCGA-LAML (top) and BEAT-AML (bottom) cohorts. I Relative ESRRA expression according to NPM1 status in the TCGAL-LAML cohort. P-value was calculated using a two-sided t-test (mean ± SD). CR complete remission.