Karyopharm reports Q2 revenue of $33.4 million, reaffirms 2026 guidance

Karyopharm Therapeutics (NASDAQ: KPTI ) reported second-quarter financial results on Thursday.

The transcript from the company's second-quarter earnings call has been provided below.

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View the webcast at Summary Karyopharm Therapeutics reported total Q2 revenue of $33.4 million, down from $37.9 million year-over-year due to the conclusion of Menarini's reimbursement of development-related expenses.

The company is focused on selinexor's potential to treat myelofibrosis, with plans to submit an sNDA based on promising data from the SENTRY trial showing improved spleen response rates and overall survival.

Karyopharm emphasized its established hematology platform to support the commercialization of selinexor in myelofibrosis, leveraging existing infrastructure from its XPOVIO product.

Management highlighted ongoing discussions with the FDA and lenders to support their financial strategy and extend cash runway, with current liquidity expected to last until September 2026.

The company reaffirmed its 2026 revenue guidance between $130 million and $150 million and discussed strategic alternatives to address upcoming debt obligations.

Full Transcript Richard (CEO) In myelofibrosis.

We are entering this next phase with a clear strategy, a focused organization, and an established hematology platform that positions us well for what lies ahead.

With that, I'll turn the call over to Reshma, who will discuss the clinical and regulatory foundation supporting our planned submission for the first-ever combination and why we believe selinexor, as a novel therapeutic mechanism, has the potential to fundamentally change the treatment of patients with myelofibrosis.

Reshma Thank you, Richard.

As Richard discussed, we believe selinexor has the potential to fundamentally change the treatment of patients with myelofibrosis.

I'd like to spend the next few minutes discussing why we believe the scientific evidence supporting that opportunity has continued to strengthen, why it supports our planned sNDA submission, and how we continue to build the clinical foundation for selinexor in myelofibrosis.

Turning to Slide 10, the biological rationale for combining XPO1 and JAK inhibition is compelling.

JAK-STAT activation is a key driver of malignant clone proliferation, splenomegaly, and disease-related symptoms, while XPO1 activity is important for malignant cell survival.

By targeting these complementary pathways simultaneously, we believe selinexor has the potential to complement JAK inhibition and improve outcomes beyond symptom control alone.

Turning to Slide 11, myelofibrosis remains a disease with a high unmet need given clinical activity with the currently approved therapies is modest.

As a result, spleen volume reduction of at least 35% is observed in less than a third of patients.

Overall survival improvements are limited and meaningful modification of the underlying disease is not observed.

Turning to Slide 12, a distinctive profile has been observed from the SENTRY trial.

Given the compelling SVR35 results that are rapid, deep, and sustained, a promising OS signal, a first-of-a-kind prediction between SVR35 and OS, and a safe and manageable adverse event profile.

These data appear to support SVR35 as a reasonably likely surrogate endpoint, enabling an sNDA under the accelerated approval pathway.

Turning to Slide 13, at Week 24 a nearly double spleen response rate was observed with the combination of selinexor plus ruxolitinib versus ruxolitinib alone.

What is particularly important is the quality and kinetics of that response.

As shown on Slide 14, the responses were rapid, emerging as early as Week 12, and deep, with greater average spleen volume reductions relative to baseline observed with the combination.

Both response rates and depth of response were sustained through Week 36.

Importantly, as seen on Slide 15, the benefit was consistent across pre-specified patient subgroups, reinforcing the robustness of the treatment effect in the vast majority of frontline myelofibrosis patients.

Especially important is a subgroup analysis by ruxolitinib dosing as seen on Slide 16.

Even with average suboptimal doses of ruxolitinib less than 15 milligrams per day, SVR35 rates with the combination were as high as 50% compared to zero observed with ruxolitinib alone, indicating that with the combination SVR35 is driven by selinexor and supported by modest doses of ruxolitinib.

From a clinical practice standpoint, these data suggest that ruxolitinib dose reductions may not compromise efficacy when combined with selinexor.

As shown on Slide 17, at the time of the top-line analysis, the overall survival hazard ratio was 0.43, and patients continue to be followed as these data mature.

On Slide 18, a post hoc landmark analysis demonstrated that irrespective of treatment, SVR35 at Week 24 predicted overall survival.

This observation is further reinforced by the longer-term follow-up from the Phase 1 trial on Slide 19, in which the same relationship between SVR35 and overall survival is observed.

On Slide 20, the importance of the SVR35—OS relationship becomes even clearer when viewed in the context of the broader myelofibrosis literature.