Rinvoq vs Jakafi
Both are JAK inhibitors. Here is how Rinvoq and Jakafi compare on class, mechanism, dosing, approval and supply.
At a glance
Key differences
- Same class. Both Rinvoq and Jakafi are JAK inhibitors, so they work through the same broad mechanism. Differences between them tend to be about dosing, route, how selective they are, and side effects rather than what they target.
- How they are taken. Both are given by the oral route.
- Time on the market. Rinvoq was first approved by the FDA in 2019, Jakafi in 2011. That gives Jakafi roughly 8 more years of real-world use and long-term safety data.
- Who markets them. Rinvoq is marketed by AbbVie; Jakafi by Incyte.
- Same drug, more than one brand. Ruxolitinib is sold as Jakafi / Jakavi — the same active ingredient marketed under different brand names, typically for different approved uses or doses.
What each one treats
RINVOQ/RINVOQ LQ is a Janus kinase (JAK) inhibitor. RINVOQ is indicated for the treatment of adults with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to one or more TNF blockers. ( 1.1 ) Limitations of Use RINVOQ is not recommended for use in combination with other JAK inhibitors, biologic DMARDs, or with potent immunosuppressants such as azathioprine and cyclosporine. ( 1.1 ) RINVOQ/RINVOQ LQ is indicated for the treatment of adults and pediatric patients 2 years of age and older with active psoriatic arthritis who have had an inadequate response or intolerance to one or more TNF blockers. ( 1.2 ) Limitation s of Use RINVOQ/RINVOQ LQ is not recommended for use in combination with other JAK inhibitors, biologic DMARDs, or with potent immunosuppressants such as azathioprine and cyclosporine. ( 1.2 ) RINVOQ is indicated for the trea…
JAKAFI/JAKAFI XR is a kinase inhibitor indicated for treatment of: intermediate or high-risk myelofibrosis, including primary myelofibrosis, post-polycythemia vera myelofibrosis, and post-essential thrombocythemia myelofibrosis in adults. ( 1.1 ) polycythemia vera in adults who have had an inadequate response to or are intolerant of hydroxyurea. ( 1.2 ) steroid-refractory acute graft-versus-host disease in adult and pediatric patients 12 years and older. ( 1.3 ) chronic graft-versus-host disease after failure of one or two lines of systemic therapy in adult and pediatric patients 12 years and older. ( 1.4 ) 1.1 Myelofibrosis JAKAFI/JAKAFI XR is indicated for treatment of intermediate or high-risk myelofibrosis (MF), including primary MF, post-polycythemia vera MF, and post-essential thrombocythemia MF in adults. 1.2 Polycythemia Vera JAKAFI/JAKAFI XR is indicated for treatment of polycy…
How each one works
12.1 Mechanism of Action Upadacitinib is a Janus kinase (JAK) inhibitor. JAKs are intracellular enzymes which transmit signals arising from cytokine or growth factor-receptor interactions on the cellular membrane to influence cellular processes of hematopoiesis and immune cell function. Within the signaling pathway, JAKs phosphorylate and activate signal transducers and activators of transcription (STATs) which modulate intracellular activity including gene expression. Upadacitinib modulates the signaling pathway at the point of JAKs, preventing the phosphorylation and activation of STATs. JAK enzymes transmit cytokine signaling through their pairing (e.g., JAK1/JAK2, JAK1/JAK3, JAK1/TYK2, …
12.1 Mechanism of Action Ruxolitinib, a kinase inhibitor, inhibits Janus Associated Kinases (JAKs), JAK1 and JAK2, which mediate the signaling of a number of cytokines and growth factors that are important for hematopoiesis and immune function. JAK signaling involves recruitment of STATs (signal transducers and activators of transcription) to cytokine receptors, activation, and subsequent localization of STATs to the nucleus leading to modulation of gene expression. MF and PV are myeloproliferative neoplasms (MPNs) known to be associated with dysregulated JAK1 and JAK2 signaling. In a mouse model of JAK2V617F-positive MPN, oral administration of ruxolitinib prevented splenomegaly, preferent…
Related comparisons
Read more
Which medicine is right for a given person depends on their diagnosis, other conditions, other medicines, kidney and liver function, pregnancy, and cost or reimbursement — none of which this page knows. Two drugs in the same class are not automatically interchangeable. Never start, stop or switch a prescription medicine on the basis of a web page; that decision belongs to you and your clinician or pharmacist.
How this page is built
The facts on this page are pulled directly from official U.S. FDA datasets — they are not written from memory. Each field below names the dataset it came from, so you can check it yourself.
- FDA Drug Label (openFDA) ↗ Indications, mechanism of action and pharmacologic class
- Drugs@FDA ↗ First FDA approval date and the company holding the application
- FDA Drug Shortage Database ↗ Current US supply / shortage status
Plain-English summaries and drug-class explainers are written and reviewed by Sreepriya Prasannan (MSc Digital Transformation of Life Sciences (Innopharma Education / Griffith College); MSc & BSc Botany). Data is retrieved automatically from the sources above and cross-checked with AI-assisted verification (Anthropic's Claude) — brand and generic names are matched against the exact FDA product record so that a combination product or a different formulation cannot be mistaken for the drug on this page. An editor reviews the result before publication. We describe this in full in our editorial standards and corrections policy. The FDA data on this page was last retrieved on 11 Oct 2026. How every register is built: methodology · fixes we have made: corrections log.