Myelofibrosis (MF), a chronic, debilitating, myeloproliferative neoplasm characterized by excessive bone marrow fibrosis, progressive hematopoietic failure, compensatory extramedullary hematopoiesis, and a reduced life expectancy, has been a one-drug-class disease for more than a decade. Since the approval of ruxolitinib (Jakafi®; Incyte) in 2011, JAK inhibitors (JAKi) are standard frontline therapy, and every subsequent myelofibrosis drug to reach the market—fedratinib (Inrebic®; Bristol Myers Squibb/BMS), pacritinib (Vonjo®; Sobi/Swedish Orphan Biovitrum), and momelotinib (Ojjaara® in the US; Omjjara® in the EU; GSK)—belong to the same mechanistic family: JAK inhibitors that suppress JAK/STAT signaling, reduce spleen size, and improve symptoms, without reliably reversing the underlying marrow fibrosis or eliminating the mutant clone driving the disease. However, to-date, only one-third of patients treated with ruxolitinib achieve a spleen volume reduction of 35% (SVR35). Despite improvements in symptoms, durable modification of underlying disease biology, including reductions in variant allele frequency (VAF), remains limited.
Key Takeaways
- Karyopharm submitted an sNDA to the FDA on August 31, 2026, seeking Accelerated Approval for selinexor (XPOVIO®) plus ruxolitinib in JAK inhibitor-naïve myelofibrosis, with Priority Review requested.
- The Phase 3 SENTRY trial met its SVR35 co-primary endpoint (49.8% vs. 28.0% with ruxolitinib alone) but did not meet its symptom-score co-primary endpoint, with both arms improving similarly.
- An early overall survival signal favored the combination (HR 0.43), but the upper bound of the confidence interval approaches 1.0, and follow-up remains immature at roughly a year.
- Accelerated Approval hinges on the FDA accepting SVR35 as a reasonably likely surrogate endpoint for survival, a determination the agency has offered in writing but not yet finalized through formal review.
- Toxicity rose meaningfully with the combination, including higher rates of grade 3 or higher adverse events and treatment discontinuations, a cost that will need to be weighed against the drug’s still-unproven survival benefit.
An estimated 20,000 patients in the United States and roughly 19,000 in the European Union live with myelofibrosis, a rare chronic blood cancer in which impaired blood-cell production and splenic enlargement can produce fatigue, abdominal discomfort, night sweats, and bone pain that persist for years.
That may, however, be about to change.
On August 31, 2026, Karyopharm Therapeutics Inc. (Nasdaq: KPTI) submitted a supplemental New Drug Application (sNDA) to the U.S. Food and Drug Administration seeking Accelerated Approval for selinexor (XPOVIO®; Karyopharm Therapeutics Inc.), an oral exportin 1 (XPO1) inhibitor already approved in multiple myeloma, in combination with ruxolitinib for JAK inhibitor-naïve patients with myelofibrosis. The company also requested Priority Review. If granted, Priority Review would shorten the FDA review period to approximately six months.[1][2]
The filing is based on the Phase 3 SENTRY trial, which produced a strong spleen-volume response, failed to demonstrate a difference in its co-primary symptom endpoint, and generated an overall survival signal that remains immature. [3][4][5][6]
What XPO1 Inhibition Is Supposed to Do That JAK Inhibition Doesn’t
Selinexor works through a mechanism distinct from JAK/STAT inhibition. XPO1 is the principal nuclear export protein responsible for transporting molecular cargo—including tumor suppressor proteins such as p53—from the nucleus into the cytoplasm. By inhibiting XPO1, selinexor promotes retention of these proteins in the nucleus, where they can continue to exert growth-regulating effects.
Preclinical studies in myelofibrosis have also implicated XPO1 inhibition in suppression of NF-κB-associated inflammatory signaling. The rationale for combining selinexor with ruxolitinib is therefore to target distinct biological pathways rather than to intensify JAK inhibition alone. Laboratory studies have reported activity of the combination against myelofibrosis cells with and without JAK2V617F or TP53 mutations.[5][7]
Selinexor is not a new molecule to oncology. It is approved in two multiple myeloma settings – in combination with bortezomib (Velcade®; Takeda) and dexamethasone (Decadron®; Merck & Co/MSD, brand discontinued in the USA) for adults who have received at least one prior therapy, and in combination with dexamethasone alone for adults with relapsed or refractory multiple myeloma who have received at least four prior therapies and whose disease is refractory to at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti-CD38 monoclonal antibody. [16]
The drug is marketed as XPOVIO® or NEXPOVIO® in more than 50 countries and territories outside the United States through commercial partners including Antengene, Menarini, Neopharm, and FORUS. Its use in myelofibrosis remains investigational. The FDA granted Orphan Drug Designation for selinexor in myelofibrosis in May 2022, followed by the European Commission’s Orphan Medicinal Product Designation in October 2022 and the FDA’s Fast Track Designation in July 2023.[1][2][16]
A Filing Built on Strong Spleen Data, Negative Symptom Data, and Immature Survival Data
SENTRY: One Primary Endpoint Was Positive. The Other Was Not
The sNDA rests on the Phase 3 portion of SENTRY (XPORT-MF-034; NCT04562389), a global, randomized, double-blind, placebo-controlled study involving 353 JAK inhibitor-naïve patients with primary or post-polycythemia vera or post-essential thrombocythemia myelofibrosis. Patients had platelet counts above 100 × 10⁹/L, spleen volumes of at least 450 cm³, and DIPSS intermediate-1 or higher risk scores. Patients were randomized 2:1 to selinexor 60 mg once weekly plus ruxolitinib or placebo plus ruxolitinib.[4][8]
SENTRY had two co-primary endpoints: the proportion of patients achieving at least a 35% reduction in spleen volume (SVR35) at week 24 and the average change in absolute total symptom score (Abs-TSS), measured using the modified Myelofibrosis Symptom Assessment Form and excluding fatigue, from baseline through week 24. The endpoints were evaluated sequentially using a one-sided alpha of 0.025.[5][8]
The trial met the spleen-volume endpoint
At week 24, 49.8% of patients receiving selinexor plus ruxolitinib achieved SVR35, compared with 28.0% receiving ruxolitinib alone. The odds ratio was 2.58 (95% CI, 1.60-4.17; one-sided P<.0001). The difference appeared early and persisted: SVR35 was achieved by 49.4% versus 20.3% of patients at week 12 and 46.9% versus 23.0% at week 36. The treatment effect was consistent across prespecified subgroups.[3][5][6][10][11][12][13]
The symptom endpoint did not meet the prespecified statistical threshold. Mean Abs-TSS improved by 9.9 points with the selinexor combination and by 10.9 points with ruxolitinib alone. The adjusted mean difference was 0.97 points (95% CI, -1.07 to 3.02; P=.825). In other words, patients in both groups experienced symptom improvement, but the addition of selinexor did not produce a statistically significant difference between treatment groups. [5][6]
That distinction matters. SENTRY was positive for one co-primary endpoint and negative for the other. The symptom result should not be described as a technical measurement failure or as evidence that patients did not improve. Patients did improve. The trial did not show greater symptom improvement with selinexor plus ruxolitinib than with ruxolitinib alone.
Encouraging, but Not Yet Definitive
Overall survival has become an important part of Karyopharm’s argument for accelerated approval. At a February 20, 2026 data cutoff, 95.3% of patients in the selinexor combination arm remained alive compared with 89.8% in the ruxolitinib-alone arm. Median follow-up was 11.6 months and 12.6 months, respectively. The reported hazard ratio for death was 0.43 (95% CI, 0.19-1.00; nominal one-sided P=.022). The Kaplan-Meier curves began to separate at approximately month 9. [3][5][6][12] The result is directionally encouraging, but it is not a mature survival analysis.
Overall survival was a secondary rather than primary endpoint of the trial; the upper boundary of the reported confidence interval is 1.00, and follow-up remains relatively short. The nominal P value should therefore not be interpreted as equivalent to a prospectively powered, multiplicity-controlled demonstration of an overall survival benefit. [5][6]
A landmark analysis provided additional context. Among patients who achieved SVR35 at week 24, 98% were alive at week 72, compared with 88% among those who did not achieve SVR35, regardless of treatment assignment. That association supports the possibility that spleen response is related to longer survival, but it does not establish that the selinexor combination itself will ultimately produce a survival benefit when follow-up is substantially longer. [5][6]
Evidence of Disease Modification?
SENTRY also included exploratory analyses of molecular response. A reduction of at least 20% in driver-mutation variant allele frequency (VAF) by week 24 occurred in 32.0% of patients receiving selinexor plus ruxolitinib, compared with 23.9% of patients receiving ruxolitinib alone. VAF reduction was associated with a greater likelihood of achieving SVR35. The combination also reduced circulating peripheral blasts in patients with detectable blasts at baseline. [5][6]
These findings are biologically interesting, particularly because they suggest activity beyond symptomatic control and spleen reduction. But they remain exploratory. Neither VAF reduction nor reduction in circulating blasts has been established as a surrogate for long-term clinical outcomes in this setting. The findings should therefore be viewed as evidence of biological activity rather than proof of disease modification that translates into longer survival.
More Toxicity
The additional efficacy came with additional toxicity. Among 234 patients evaluable for safety in the combination arm and 116 in the ruxolitinib-alone arm, the most common all-grade treatment-emergent adverse events with selinexor plus ruxolitinib were thrombocytopenia (59% versus 43%), anemia (57% versus 58%), nausea (57% versus 17%), constipation (32% versus 36%), and neutropenia (27% versus 9%). [5][6] Grade 3 or higher adverse events occurred in 70.1% of patients receiving the combination, compared with 50.0% of patients receiving ruxolitinib alone. Individual grade 3 or higher adverse events in the combination arm included anemia in approximately 37% of patients, thrombocytopenia in 18%, neutropenia in 16%, nausea in 7%, and fatigue in 6%. [5][6]
Treatment discontinuation due to adverse events occurred in 14.5% of patients receiving the combination versus 8.6% of those receiving ruxolitinib alone. Acute myeloid leukemia progression occurred in 1.7% of patients in each treatment group.[5][6] The toxicity profile is relevant to the regulatory decision because patients with myelofibrosis may already have clinically significant cytopenias from the underlying disease and may be receiving ruxolitinib at reduced doses because of hematologic toxicity.
The Phase 1 Foundation: Why 60 mg?
The Phase 3 program followed an earlier open-label Phase 1 study published in Blood Advances in May 2026. That study enrolled 24 JAK inhibitor-naïve patients with myelofibrosis and evaluated selinexor at 40 mg or 60 mg once weekly in combination with ruxolitinib.[7]
No dose-limiting toxicities were observed at either dose, and a maximum tolerated dose was not formally established. The Phase 3 dose was selected using safety, efficacy, and pharmacokinetic exposure-response data. [7]
The 60-mg dose produced the stronger response rates in the Phase 1 study. At week 24, SVR35 was achieved in 11 of 14 patients (79%) receiving 60 mg and 4 of 10 patients (40%) receiving 40 mg. TSS50 was achieved in 7 of 12 patients (58%) at 60 mg and 4 of 10 patients (40%) at 40 mg. [7]
A small subgroup receiving a suboptimal ruxolitinib dose of 5 mg or less twice daily also showed high response rates when selinexor 60 mg was added. SVR35 was observed in 6 of 6 patients, and TSS50 in 3 of 4 evaluable patients. Because these numbers were very small, the findings should be interpreted with caution.[7] The difference between the Phase 1 and Phase 3 response rates is also important. The Phase 1 study involved only 24 patients and was open-label and uncontrolled. SENTRY enrolled 353 patients in a randomized, double-blind comparison against ruxolitinib plus placebo. At the Phase 3 dose, SVR35 was 49.8%, substantially lower than the 79% observed in the 60-mg Phase 1 cohort.[5][7]
The Phase 3 result provides a more reliable estimate of the treatment effect because of its larger, randomized, blinded design. The smaller Phase 1 study established the direction of activity and supported dose selection, but its response rate should not be treated as the expected outcome for the broader Phase 3 population.
Reliance on SVR35
Karyopharm’s accelerated-approval strategy depends on SVR35. Before filing the sNDA, the company disclosed that the FDA had provided written feedback indicating that SVR35 appears to qualify as a reasonably likely surrogate endpoint (RLSE) for overall survival in this setting. If that position is maintained during formal review, the spleen-volume response could support accelerated approval before the overall survival data mature.[1][2] Karyopharm confirmed it intends to continue long-term follow-up of SENTRY’s overall survival data as confirmatory evidence. The trial remains blinded and does not include a crossover provision.[1][3]
The distinction between the FDA’s pre-submission feedback and an actual regulatory determination is important. The agency has not yet approved selinexor plus ruxolitinib for myelofibrosis, and the formal sNDA review will determine whether SVR35 is sufficient to support accelerated approval in this setting.[1][2] The company expects an FDA decision on whether the sNDA has been accepted for filing during the fourth quarter of 2026, following the agency’s standard 60-day filing review period. If Priority Review is granted, the company expects a review period of approximately six months following acceptance.[1][2]
Other Ruxolitinib Combinations
Selinexor is entering a development landscape in which other non-JAK agents have already been tested in combination with ruxolitinib.
Pelabresib plus ruxolitinib, evaluated in the MANIFEST-2 Phase 3 study, and navitoclax plus ruxolitinib, evaluated in TRANSFORM-1, both improved SVR35 compared with ruxolitinib alone in their respective Phase 3 trials. Neither combination demonstrated an improvement in symptom scores over ruxolitinib alone, nor did either improve anemia.[14][15] These results provide useful context but do not establish that one combination is superior to another. The studies were conducted separately and were not head-to-head comparisons.
A 2026 systematic review and meta-analysis covering 19 studies and 1,088 patients reported that selinexor plus ruxolitinib had the highest SVR35 and TSS50 response rates among ruxolitinib-based combinations in JAK inhibitor-naïve patients. However, the analysis incorporated the small Phase 1 selinexor dataset rather than the Phase 3 SENTRY results. Cross-trial comparisons, therefore, remain limited by differences in study populations, designs, endpoints, and follow-up periods.[9]
What Remains Open
Several questions remain between the SENTRY results and an FDA approval decision.
- First, the trial failed to meet one of its two co-primary endpoints. Patients receiving both treatments improved symptomatically, but the addition of selinexor did not yield a statistically significant improvement in Abs-TSS compared with ruxolitinib alone.[5][6].
- Second, the overall survival result remains immature. The hazard ratio of 0.43 is encouraging, but the 95% confidence interval extends to 1.00, follow-up is approximately one year, and overall survival was not the trial’s primary endpoint.[5][6]
- Third, the regulatory significance of SVR35 remains to be established through formal FDA review. Karyopharm has reported positive written feedback from the agency regarding SVR35 as a reasonably likely surrogate endpoint, but that feedback is not the same as an approval decision. [1][2]
- Finally, the combination adds clinically meaningful toxicity. Grade 3 or higher adverse events occurred in 70.1% of patients, compared with 50.0% with ruxolitinib alone, and treatment discontinuation due to adverse events increased from 8.6% to 14.5%.[5][6]
Those risks will need to be weighed against the magnitude and durability of spleen response and, ultimately, against whether the emerging survival signal persists with longer follow-up.
A Filing Built on Strong Spleen Data, Negative Symptom Data, and Immature Survival
Karyopharm’s filing could mark the first regulatory step toward approval of a myelofibrosis combination built around a mechanism other than JAK inhibition. The SENTRY spleen-volume data provide a substantial basis for that argument: 49.8% of patients achieved SVR35 at week 24 with selinexor plus ruxolitinib compared with 28.0% with ruxolitinib alone, and the difference persisted through week 36.[5,6]
The symptom endpoint was different. The combination did not outperform ruxolitinib alone on the prespecified Abs-TSS endpoint.
The overall survival analysis is encouraging but remains preliminary. A hazard ratio of 0.43, with a confidence interval extending to 1.00 and approximately one year of follow-up, is not yet enough to establish a durable survival benefit. The FDA will now determine how those findings fit together. The central regulatory question is whether the SVR35 result can serve as a reasonably likely surrogate for overall survival and support accelerated approval while the survival data mature. The agency will also have to consider the negative symptom endpoint and the additional toxicity associated with adding selinexor.
For a disease that has relied on JAK inhibition since 2011, the possibility of a second mechanistic approach is significant. Whether selinexor plus ruxolitinib becomes that second approved approach will depend on what the FDA concludes from the complete SENTRY record—and on whether the survival signal remains intact as the trial continues to mature.
Note: The published abstract of the Phase 1 study reports week-24 response rates of 38% for SVR35 and 25% for TSS50 in the selinexor 40-mg plus ruxolitinib group. However, the same paper (Table 3) reports that 4 of 10 patients achieved SVR35 and 4 of 10 achieved TSS50, corresponding to 40% for each endpoint. The Results section also reports 4/10 (40%) for both endpoints. The 60-mg results are consistent between the abstract and Table 3 at 79% for SVR35 and 58% for TSS50. Accordingly, this article uses the patient-count-derived figures from the table and the Results section rather than reproducing the discrepant percentages in the abstract. Published Phase 1 study
Summary: What Clinicians Know About Selinexor Today
Selinexor already has an established FDA safety profile in multiple myeloma, although that experience does not substitute for a myelofibrosis-specific indication for use.
The current FDA-approved indications are:
- In combination with bortezomib and dexamethasone (XVd) for adults with multiple myeloma who have received at least one prior therapy.
- In combination with dexamethasone (Xd) for adults with relapsed or refractory multiple myeloma who have received at least four prior therapies and whose disease is refractory to at least two proteasome inhibitors, at least two immunomodulatory agents, and an anti-CD38 monoclonal antibody. [16]
The prescribing information includes warnings and precautions for thrombocytopenia, neutropenia, gastrointestinal toxicity, hyponatremia, serious infections, neurological toxicity, embryo-fetal toxicity, and cataracts. The label recommends regular monitoring of blood counts and serum sodium, as well as antiemetic prophylaxis to reduce gastrointestinal toxicity. [16]
In the XVd setting, adverse reactions occurring in at least 20% of patients include fatigue, nausea, decreased appetite, diarrhea, peripheral neuropathy, upper respiratory tract infection, decreased weight, cataract, and vomiting. In the pivotal BOSTON study, fatal adverse reactions occurred in 6% of patients within 30 days of the last treatment, serious adverse reactions occurred in 52%, and 19% discontinued treatment because of adverse events. [16]
In the Xd setting, common adverse reactions include thrombocytopenia, fatigue, nausea, anemia, decreased appetite, decreased weight, diarrhea, vomiting, hyponatremia, neutropenia, leukopenia, constipation, dyspnea, and upper respiratory tract infection. In the STORM study, fatal adverse reactions occurred in 9% of patients, serious adverse reactions in 58%, and 27% of patients discontinued treatment because of adverse events.[16]
The SENTRY safety profile—70.1% of patients experienced grade 3 or higher adverse events, with a 14.5% discontinuation rate—falls within the range already seen with selinexor in multiple myeloma. However, myelofibrosis is a distinct disease population, and any eventual indication for myelofibrosis would require its own safety assessment.[5][16]
Clinical Trials
- Study of Selinexor in Combination With Ruxolitinib in Myelofibrosis (SENTRY / XPORT-MF-034) – ClinicalTrials.gov ID NCT04562389 [4][8]
- Selinexor in Myelofibrosis Refractory or Intolerant to JAK1/2 Inhibitors (ESSENTIAL) – ClinicalTrials.gov ID NCT03627403
- A Study of Selinexor Monotherapy in Subjects With JAK Inhibitor-naïve Myelofibrosis and Moderate Thrombocytopenia (SENTRY-2 / XPORT-MF-044) – ClinicalTrials.gov ID NCT05980806
Highlights of Prescribing Information
Selinexor (XPOVIO®; Karyopharm Therapeutics)[Prescribing Information]
Ruxolitinib (Jakafi®; Incyte) [Prescribing Information]
Fedratinib (Inrebic®; Bristol Myers Squibb/BMS) [Prescribing Information]
Pacritinib (Vonjo®; Sobi/Swedish Orphan Biovitrum) [Prescribing Information]
Momelotinib (Ojjaara® in the US; Omjjara® in the EU; GSK) [Prescribing Information]
References
[1] Karyopharm Therapeutics Inc. Karyopharm Submits Supplemental New Drug Application to the FDA for XPOVIO® (selinexor) Plus Ruxolitinib for Patients with Myelofibrosis. Press release, August 31, 2026. PR Newswire
[2] Karyopharm Therapeutics Inc. Karyopharm Plans to Submit sNDA for Selinexor Plus Ruxolitinib in Myelofibrosis Under Accelerated Approval Pathway. Press release, July 30, 2026. PR Newswire
[3] Karyopharm Therapeutics Inc. Karyopharm to Present Results from Phase 3 SENTRY Trial of Selinexor Plus Ruxolitinib in Myelofibrosis in Late-Breaking Oral Presentation at ASCO 2026 with Simultaneous Publication in the Journal of Clinical Oncology. Press release, June 2, 2026. Karyopharm Investor Relations
[4] ClinicalTrials.gov. Study of Selinexor in Combination With Ruxolitinib in Myelofibrosis (SENTRY). NCT04562389. ClinicalTrials.gov
[5] Bose P, Ali H, Al-Ali HK, Garcia-Gutierrez V, Grosicki S, Grudeva-Popova Z, Harrison C, Hong J, Hou HA, Kwiatek M, Loschi M, Passamonti F, Patriarca A, Podoltsev N, Rampal R, Tantravahi S, Urian LG, Chai Y, Taverna P, Mark T, Sadiq A, Rangwala R, Vachhani P, Mascarenhas J; SENTRY Trial Investigators. Selinexor Plus Ruxolitinib in Janus Kinase Inhibitor-Naïve Myelofibrosis: Phase III SENTRY Trial. J Clin Oncol. 2026 Aug;44(22):2098-2109. doi: 10.1200/JCO-26-01080. Epub 2026 Jun 2. Erratum in: J Clin Oncol. 2026 Sep;44(25):2465. doi: 10.1200/JCO-26-01827. PMID: 42227656; PMCID: PMC13440559. Journal of Clinical Oncology
[6] Mascarenhas J, et al. Selinexor plus ruxolitinib in JAK inhibitor-naïve myelofibrosis: Phase 3 SENTRY trial [abstract LBA6500]. J Clin Oncol. 2026;44(17_suppl). DOI: 10.1200/JCO.2026.44.17_suppl.LBA6500.
[7] Ali H, Mohan S, Kishtagari A, Prchal JT, Maher K, Chai Y, Gudi G, Taverna P, Mark T, Tantravahi SK. Selinexor plus ruxolitinib in JAK inhibitor-naïve patients with myelofibrosis: a multicenter, open-label, phase 1 study. Blood Adv. 2026 May 26;10(10):3383-3397. doi: 10.1182/bloodadvances.2025018706. PMID: 41785311; PMCID: PMC13194599. PubMed Central
[8] Mascarenhas J, Maher K, Rampal R, Bose P, Podoltsev N, Hong J, Chai Y, Kye S, Method M, Harrison C; SENTRY investigators. Selinexor plus ruxolitinib in JAK inhibitor treatment-naïve myelofibrosis: SENTRY Phase 3 study design. Future Oncol. 2025 Mar;21(7):807-813. doi: 10.1080/14796694.2025.2461393. Epub 2025 Feb 6. PMID: 39911057; PMCID: PMC11916360. PubMed Central
[9] Tan S, Li Y, Cao Y, Sun W, Hui W. Efficacy and safety of Ruxolitinib-based combination therapy in the patients with Myelofibrosis (MF): a systematic review and meta-analysis. Ann Med. 2026 Dec;58(1):2634532. doi: 10.1080/07853890.2026.2634532. Epub 2026 Feb 27. PMID: 41761659; PMCID: PMC12951650. PubMed Central
[10] OncLive. FDA sNDA Submission Is Planned for Selinexor Plus Ruxolitinib in Myelofibrosis. 2026. OncLive
[11] Targeted Oncology. FDA Approval Sought for Selinexor Plus Ruxolitinib in Myelofibrosis. 2026. Targeted Oncology
[12] Targeted Oncology. Selinexor Plus Ruxolitinib Improves Spleen Responses, Shows OS Signal in Frontline Myelofibrosis. 2026. Targeted Oncology
[13] touchONCOLOGY / touchHAEMATOLOGY. Phase 3 SENTRY trial positions selinexor plus ruxolitinib as potential new frontline option in myelofibrosis. July 1, 2026. touchONCOLOGY
[14] Rampal RK, Grosicki S, Chraniuk D, Abruzzese E, Bose P, Gerds AT, Vannucchi AM, Palandri F, Lee SE, Gupta V, Lucchesi A, Oh ST, Kuykendall AT, Patriarca A, Álvarez-Larrán A, Mesa R, Kiladjian JJ, Talpaz M, Scandura JM, Lavie D, Harris M, Kays SK, Li Q, Boxhammer R, Brown B, Jegg AM, Harrison CN, Mascarenhas J. Pelabresib plus ruxolitinib for JAK inhibitor-naive myelofibrosis: a randomized phase 3 trial. Nat Med. 2025 May;31(5):1531-1538. doi: 10.1038/s41591-025-03572-3. Epub 2025 Mar 10. PMID: 40065169; PMCID: PMC12092244.
[15] Pemmaraju N, Mead AJ, Somervaille TC, McCloskey JK, Palandri F, Koschmieder S, Lavie D, Leber B, Yeh S, Gómez-Casares MT, Ammatuna E, Shin H, Kirito K, Jourdan É, Devos T, Chuah HS, Radinoff A, Bogdanovic A, Moskal R, Jiang Q, Chopra AS, Papadopoulos E, Potluri J, Passamonti F.. Transform-1: A Randomized, Double-Blind, Placebo-Controlled, Multicenter, International Phase 3 Study of Navitoclax in Combination with Ruxolitinib Versus Ruxolitinib Plus Placebo in Patients with Untreated Myelofibrosis. Blood. 2023;142(suppl 1):620.
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