Ipsen buys Kartos in $1.75bn myelofibrosis push
Paris-based Ipsen has agreed to acquire US biotech Kartos Therapeutics in a deal worth up to $1.75bn, adding a late-stage blood cancer programme to its growing oncology pipeline.
Why it matters: The deal gives Ipsen navtemadlin, an oral MDM2 inhibitor in Phase III development for myelofibrosis, a rare bone marrow cancer where many patients respond only partially to the current standard treatment ruxolitinib, a JAK inhibitor sold by Novartis in Europe under the brand name Jakavi.
- Ipsen will pay $450m upfront, with Kartos shareholders eligible for up to $1.3bn in regulatory and sales-based milestones.
Zoom in: Navtemadlin is being tested as an add-on to ruxolitinib in patients with intermediate- and high-risk TP53 wild-type myelofibrosis who have a suboptimal response to the JAK inhibitor.
- The pivotal Phase III POIESIS trial is expected to enrol more than 600 patients across more than 250 sites, with topline data expected in 2027. Ipsen’s CEO, David Loew, said the drug could offer a new treatment option as early as 2028.
How it works: MDM2 is a negative regulator of p53, one of the body’s most important tumour suppressor proteins. By blocking MDM2, navtemadlin is designed to restore p53 activity and push cancer cells towards apoptosis.
- This approach depends on patients retaining wild-type TP53, the naturally occurring, non-mutated version of the TP53 gene, which is why patient selection is central to the programme.
- In April 2021, Kartos announced a partnership with Illumina to develop a sequencing-based TP53 companion diagnostic, which we can assume will be central to the POIESIS trial recruitment.
By the numbers: Earlier Phase Ib/II data in patients with suboptimal response to ruxolitinib showed that 32% achieved at least a 35% spleen volume reduction at week 24, while 32% achieved a 50% or greater improvement in total symptom score.
- Ipsen also highlighted biomarker signals suggesting potential disease modification, including reductions in driver variant allele frequency and improvements in bone marrow fibrosis in a small evaluable group.
What we’re watching: The Kartos deal is Ipsen’s second recent move to deepen its blood cancer pipeline. In October 2025, the French pharma agreed to acquire ImCheck Therapeutics, adding a late-stage monoclonal antibody programme in acute myeloid leukaemia.
Backstory: MDM2 inhibition has had a long and uneven development history. The rationale is elegant: reactivate p53 in cancers where the gene is still intact but functionally suppressed. The challenge has been turning that biology into tolerable and clinically meaningful drugs.
- Recent work in myelofibrosis has revived interest in the class, particularly in combination with JAK inhibition. Novartis’ siremadlin is another prominent MDM2 inhibitor being explored in myelofibrosis combinations, although navtemadlin appears to be the more advanced registrational-stage asset in this setting.
Yes, but: MDM2 inhibitors still carry known risks, especially haematologic toxicity. In the broader class, researchers have also flagged the need to monitor clonal evolution, including the emergence of TP53-altered clones during treatment.
The bottom line: Ipsen is making a calculated bet that MDM2 inhibition is finally ready for prime time in myelofibrosis. If POIESIS reads out positively in 2027, the Kartos deal could give Ipsen a differentiated late-stage oncology launch. If not, it will be another reminder that p53 reactivation has always been more compelling in biology than easy in the clinic.
