Inrebic (fedratinib)

Similarly, ectopic expression of survivin, vimentin, or cyclin D1 partially rescued the phenotypic changes induced by fedratinib. Fedratinib exerts antitumor effects against ESCC in vitro, in vivo, and in patient-derived organoid models by suppressing the JAK2-STAT3 signaling axis and its downstream effectors, vimentin, survivin, and cyclin D1.

P2, N=30, Active, not recruiting, Institut für Klinische Krebsforschung IKF GmbH at Krankenhaus Nordwest | Trial primary completion date: Dec 2025 --> Mar 2026

Fedratinib exhibits therapeutic duality: inhibition of SRC and JAK2 attenuates fibrosis by inhibiting JAK-STAT/TGFβ/Smad3 pathways, while off-target binding to AKT1/EGFR drives renal injury and vitamin B1 depletion-related toxicity with black-box encephalopathy warning. Evidence suggests for CKD patients with estimated glomerular filtration rate (eGFR) <45 mL/min/1.73 m2 or age ≥70 years, a 50% dose reduction (200 mg/day) with renal function and thiamin monitoring (<30 nmol/L) may optimize risk-benefit profile.

P2, N=20, Recruiting, Fred Hutchinson Cancer Center | Suspended --> Recruiting

Equally, there is a major focus on next generation JAK inhibitors and mutant calreticulin antibodies. There is also increasing conversation around the need for novel endpoints, as the limitations of symptom assessment, in particular, become apparent and candidate biomarkers of disease modification emerge.

All JAKi reduced EC inflammation but most JAKi could not prevent the up-regulation of adhesion molecules or the increase in procoagulant and the decrease in anticoagulant factors triggered by proinflammatory cytokines. Peficitinib and fedratinib exhibited cytotoxic effects causing EC apoptosis.

Telmisartan was used as the internal standard (IS). Stability studies confirmed the analyte's integrity across multiple freeze-thaw cycles. The developed LC-MS/MS method is selective, sensitive, fully validated, and was successfully applied to pharmacokinetic studies.

This process can be inhibited by the drug TG-101348. We constructed a risk model with three chemokine-related genes (CRGs), which could effectively predict the prognosis of THCA. Notably, CCL17 expression had a considerable value to the risk model and may promote THCA progression by regulating the JAK-STAT pathway.

P1/2, N=31, Active, not recruiting, Bristol-Myers Squibb | Trial completion date: Oct 2025 --> Nov 2026

P2, N=20, Suspended, Fred Hutchinson Cancer Center | Recruiting --> Suspended | Trial primary completion date: Aug 2026 --> Apr 2027

Nearly 50% of PMF patients experience anemia (hemoglobin (Hb) < 10 g/dL), often worsened by JAK inhibitors like ruxolitinib and fedratinib. However, heterogeneity in control groups limited direct efficacy comparisons. Larger studies are needed to confirm its effectiveness and safety.