Background: Idiopathic pulmonary fibrosis (IPF) is a progressive disorder of fibrosing interstitial lung disease with variable courses of the disease. Emerging evidence suggests a correlation between immunometabolic remodeling of myeloid cells in the blood and fibrosis severity and progression. Succinate is capable of signaling metabolite, and HIF-1 and 1 alpha unifies metabolic and inflammatory stress response, providing an inviting axis which is relevant to fibrosis biology. Objective: To assess the discriminatory ability of serum succinate and PBMC HIF-1 alpha (and a composite score with succinate and HIF alpha Information [Successful discrimination]), of fibrosis severity and progression in IPF compared to controls. Methods: A case Butler clinical biomarker research capable of 100 medical sombre stages in the pattern of 50 are observed with IPF and the other 50 to serve as a control person. Serum succinate and cytokines (IL-1 beta, TNF alpha and TGF beta 1) were measured by enzyme immunoassay (ELIZA). HIF-1a was analyzed in lysates of the PBMCs (normalized on total protein). The severity of fibrosis was measured by HRCT fibrosis extent score, FVC% predicted, and DLCO% predicted. Group comparisons were performed using t-tests or a Mann-Whitney U tests as appropriate and categorical variables were performed using chi-square tests. Associations with severity were evaluated by using Spearman correlations and multivariable linear regression with age, sex, BMI and smoking. Progression risk was assessed in IPF by stable vs progressive classification, ROC/AUC statistical analyses and adjusted logistic regression. Results: Baseline characteristics were similar between groups (age, BMI, sex and ever-smoking; all p> 0.05). IPF had significantly increased serum Succinate (median, 3.14 [3.00-3.49] vs 2.24 [2.06-2.35] umol/l; p < 0.001) and PBMC HIF-1a (187.6 (+-21.6) vs 129.3 (+-27.2) pg/mg protein; P < 0.001). IL-1 beta and TNF alpha were up in IPF (both p<0.001) and TGF beta 1 slightly (p=0.013). Succinate was associated with HRCT score (rho=0.734, p<0.001), FVC% (rho=-0.480, p<0.001) and DLCO% (rho=-0.612, p<0.001) in IPF. A positive correlation was found between HIF-1a and HRCT (rho=0.360, p=0.010) and DLCO% (rho=-0.343, p=0.015). In adjusted models, succinate was independently associated with HRCT (bet (adjusted) = 13.991 per 1umol/L; p<0.001) and DLCO% (bet = -22.633; p<0.001), whereas HIF-1alpha was independently associated with HRCT (beta = 0.839 per 10 pg/mg; p=0.011) and DLCO% (beta = -1.207; p=0.013). Progression analysis revealed an increase in PBMC HIF-1a (p=0.003) and increase in axis score (p=0.008) during progressive disease. ROC analyses revealed the AUC value of succinate (0.608), HIF-1 alpha (0.794), and the axis score (0.755). Axis score was found to be an independent predictor of progression (OR = 3.33 per 1 SD; p= 0.012). Conclusion: The modelled results confirm the hypothesis that succinate and PBMC HIF-1 alpha are immunometabolic phenotype indicators related to the severity of IPF and that PBMC HIF-1 alpha and Succinate-HIF axis score are stronger signal for progression risk. Validation in external, real-world cohorts, assay harmonization and longitudinal replication are needed before the clinical translocation.