Srdan Verstovsek, MD, PhD

Srdan Verstovsek, MD, PhD, a professor of Medicine and a hematologic oncologist at the University of Texas MD Anderson Cancer Center, discusses the increased thrombotic risk and management for patients with essential thrombocythemia (ET).

Patients who are at high-risk of developing blood clotting are those older than the age of 60 and those who have a JAK2 mutation. Additionally, those who have a history of blood clotting are at an increased thrombotic risk.

Verstovsek notes that a current standard practice for these patients is to prescribe hydroxyurea to decrease the blood cell count and anagrelide (Agrylin) in the second-line.

In essential thrombocythemia or ET, we worry about the thrombotic risk and our priority is to decrease it. We define the patients that are at an increased risk of blood clotting by applying certain prognostic factors. A significant change in the prognostication happened several years ago, which is now incorporated in United States based guidance, the NCCN guidelines. This is to say that in addition to historical factors of age over 60, or history of blood clotting, now, we also account for a presence or absence of a JAK2 mutation, which is present in about 60% of ET patients and it drives the disease process.

Therefore, there is a significant shift in identifying those that are at high risk of blood clotting by adding a JAK2 mutation presence to age. So patients that are older than 60 and have a JAK2 mutation are the high-risk patients or of course, those that have a history of blood clotting. There is also an attempt to improve our management of these patients. Standard practice is to prescribe hydroxyurea, which is chemotherapy by mouth, to decrease the blood cell count. Then anagrelide is a second-line agent which inhibits the growth of the cells in the bone marrow that make platelets, so it lowers the platelets.

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Srdan Verstovsek, MD, PhD, discusses the increased thrombotic risk and management for patients with essential thrombocythemia.


Increased Thrombotic Risk in Essential Thrombocythemia

Srdan Verstovsek, MD, PhD, a professor of Medicine and a hematologic oncologist at the University of Texas MD Anderson Cancer Center, highlights what future research in myeloproliferative neoplasms looks to examine.


Advancements in developing novel therapeutic strategies are underway for the treatment of patients with myelofibrosis, polycythemia vera, and essential thrombocythemia.


According to Verstovek, ongoing trials are evaluating JAK inhibitors, combination therapies, and other ways for patients to achieve partial or complete responses. The primary goal is to prolong overall survival for these patients.

We are looking first to see whether the combinations that are exploring enhancement of the control of the sign symptoms, on top of JAK inhibitors, will actually do that well or well enough to be approved and considered everyday practice. We are also looking in the very near future to see whether any of these therapies can prolong life. Overall survival is already in 1 study with a possible approval with the drug called imetelstat, which is a telomerase inhibitor, a primary goal. This is a phase 3 randomized study in a second-line setting.

Then to enhance that, perhaps not in a year but in 3-5 years, that effect of the potential targeted agents to bring about the molecular response, and that would mean possibly a complete response and partial response. We are at the beginning of the new phase in developing the drugs, not just to talk about improvement in the number or the size of the spleen or a blood cell count, but also to talk about affecting the malignant clone.

Srdan Verstovsek, MD, PhD, highlights what future research in myeloproliferative neoplasms looks to examine.

Future Directions for MPN Research

Myelofibrosis (MF), the most aggressive myeloproliferative neoplasm (MPN), is witnessing a meteoric rise in the clinical development of novel treatments in light of the dramatic impact of ruxolitinib (Jakafi) and other advancements. Ruxolitinib was the first JAK1/2 inhibitor that received regulatory approval and became the cornerstone MF treatment by improving quality of life and significantly prolonging survival of patients with MF.

 Fedratinib (Inrebic), the second JAK2 inhibitor that received regulatory approval in 2019, may be a good second-line option for ruxolitinib-resistant patients with intermediate-2 and high-risk MF.

Notably, the unmet need of severely thrombocytopenic patients with intermediate- or high-risk MF was addressed with the recent regulatory approval of pacritinib (Vonjo), a JAK2/IRAK1 inhibitor.

Splenomegaly, anemia, and constitutional symptoms are hallmarks of MF. Momelotinib, the first JAK1/2 inhibitor with the exclusive attribute to simultaneously improve anemia by suppressing hepcidin expression in the liver via ACVR1/ALK2 inhibition

 while also improving splenomegaly and constitutional symptoms, is in advanced clinical development for anemic and symptomatic patients with MF. Momelotinib demonstrated significant improvements in anemia measures, spleen size, and symptoms

 in the ongoing pivotal phase 3 MOMENTUM trial (NCT04173494)

evaluating JAK-inhibitor treated, symptomatic, and anemic patients with MF. Momelotinib’s marked anemia benefits, including achievement of red blood cell (RBC) transfusion independence

appear to underlie prolongation of survival in those with MF.

 Momelotinib may receive regulatory approval as a treatment for anemic patients with MF in the near future.

Notwithstandingthe remarkable benefits of JAK inhibitors,

many novel treatments, acting through various mechanisms, are being explored either as single agents or in combination with ruxolitinib.

Design and development of new strategies to treat MF aim at addressing unmet therapeutic needs, including suboptimal response or resistance to JAK inhibitors, cytopenias, progressive disease, achieving deeper spleen and symptom responses, prolongation of survival, and disease modification.

During the MPN session at the 10th Annual Meeting of the Society of Hematologic Oncology (SOHO 2022), Srdan Verstovsek, MD, PhD, United Energy Resources, Inc, Professor of Medicine and hematologist oncologist at The University of Texas MD Anderson Cancer Center, will highlight recent advancements in developing novel therapeutic strategies for MF during the Myeloproliferative Neoplasms Session on September 29, 2022.

Therapies Combined with Ruxolitinib in the Frontline

Luspatercept (Reblozyl) is an activin receptor-ligand trap molecule. In the phase 2 trial on luspatercept (NCT03194542) in patients with transfusion-dependent MF, 46% of them on a stable dose of ruxolitinib also receiving luspatercept had a 50% or greater decrease in RBC transfusion burden and 36% achieved transfusion-independence for 12 or more consecutive weeks.

 Currently, luspatercept is being evaluated in the registrational phase 3 INDEPENDENCE trial (NCT04717414) in patients with MF who are concomitantly treated with ruxolitinib and require RBC transfusions.

Dual inhibition of the JAK/STAT and BET pathways demonstrated synergism in preclinical studies and may be a promising strategy to enhance the efficacy of ruxolitinib in MF.

In the phase 2 MANIFEST study (NCT02158858), pelabresib (formerly CPI-0610), a first-in-class, oral, selective BET (epigenetic modifier) inhibitor, was combined with ruxolitinib. The combination elicited 35% or greater spleen volume reductions (SVR35) and 50% or greater improvement in total symptom score (TSS50) from baseline in 68% and 56% of the enrolled JAK inhibitor-naïve patients with MF (Arm 3), respectively, at 24 weeks.

were significantly higher than historical data reported for ruxolitinib monotherapy in phase 2 and 3 trials.

 Pelabresib in combination with ruxolitinib is being evaluated in the global, registrational phase 3 MANIFEST-2 trial (NCT04603495) in JAK inhibitor-naïve patients.

Navitoclax (formerly ABT-263) inhibits the anti-apoptotic BCL-2 family of proteins (primarily BCL-XL) and may enhance the clinical activity of ruxolitinib based on preclinical studies. In the phase 2 REFINE study (NCT03222609; cohort 3), navitoclax combined with ruxolitinib achieved spleen and symptom responses, and improved anemia and bone marrow fibrosis in a significant number of JAK inhibitor-naïve patients.

 Currently, navitoclax combined with ruxolitinib is being evaluated in JAK inhibitor-naïve patients in the phase 3 trial TRANSFORM-1 (NCT04472598).

“Add-on” Agents to Ruxolitinib in the Second-Line Setting

Navitoclax in combination with ruxolitinib has also been evaluated in the second-line setting in MF patients. In the phase 2 REFINE trial (cohort 1a), a significant number of patients with MF treated with the combination navitoclax/ruxolitinib achieved SVR35 and TSS50 compared with baseline at week 24, and bone marrow fibrosis improved by at least 1 grade in about one-third of ruxolitinib-treated patients

 Patients who had 1 grade or higher improvement in bone marrow fibrosis and 20% or greater reduction in allele burden of driver mutations demonstrated prolonged survival.

Navitoclax in combination with ruxolitinib is undergoing investigation in the randomized phase 3 trial TRANSFORM-2 (NCT04468984) in the second line.

A potent and highly selective inhibitor of PI3 kinase, parsaclisib, was assessed as an “add-on” agent to ruxolitinib in patients with MF and a suboptimal response to ruxolitinib. The combination parsaclisib/ruxolitinib will be explored in the phase 3 trial, LIMBER-304 (NCT04551053), in those with MF who had suboptimal response to ruxolitinib.

Navtemadlin (formerly KRT-232) is a first-in-class, potent, bioavailable inhibitor of HDM2, a key negative regulator of p53. This drug demonstrated encouraging clinical efficacy and tolerability in 

 wild-type patients with MF who failed ruxolitinib in a phase 2 study. Navtemadlin will be compared to best available therapy (BAT), excluding JAK inhibitors, in the global phase 3 BOREAS trial (NCT03662126) in 

 wild-type patients who are refractory or resistant to JAK inhibitors.

Lastly, imetelstat, a first-in-class potent telomerase inhibitor, yielded a median overall survival of 29.

 months (dose, 9.4 mg/kg) in patients with intermediate-2 or high-risk MF relapsed/refractory to JAK inhibitors in the phase 2 IMbark study (NCT02426086).

The overall survival benefit from imetelstat compared favorably with matched historical data for treatment with BAT after JAK inhibitor failure. The international, registrational phase 3 trial IMpactMF (NCT04576156) is underway to evaluate the potential survival advantage—an unprecedented trial end point for investigational MF therapies—of imetelstat in intermediate-2 or high-risk JAK inhibitor–refractory MF.

In addition to the transformative impact of JAK inhibitors in the MPN landscape and their central role in treating MF,

 several promising novel agents with various mechanisms of action—administered as monotherapies or in combination with ruxolitinib—are in advanced clinical development.

 These strategies are poised to expand the armamentarium of MF therapeutics with novel disease-modifying agents that complement the clinical benefits of ruxolitinib (eg, depth and duration of spleen, symptom responses), improve other aspects of the disease besides splenomegaly and constitutional symptoms (eg, bone marrow fibrosis, driver mutation burden), address unmet needs in MF (eg, cytopenias, resistance to ruxolitinib), and prolong survival.

1. Masarova L, Bose P, Pemmaraju N, et al. Improved survival of patients with myelofibrosis in the last decade: single-center experience. 

. 2022;128(8):1658-1665. doi:10.1002/cncr.34103

2. Verstovsek S, Parasuraman S, Yu J, et al. Real-world survival of US patients with intermediate- to high-risk myelofibrosis: impact of ruxolitinib approval. 

. 2022;101(1):131-137. doi:10.1007/s00277-021-04682-x

3. Harrison CN, Schaap N, Vannucchi AM, et al. Fedratinib in patients with myelofibrosis previously treated with ruxolitinib: An updated analysis of the JAKARTA2 study using stringent criteria for ruxolitinib failure. 

. 2020;95(6):594-603. doi:10.1002/ajh.25777

4. Verstovsek S, Mesa R, Talpaz M, et al. Retrospective analysis of pacritinib in patients with myelofibrosis and severe thrombocytopenia. 

 2022;107(7):1599-1607. doi:10.3324/haematol.2021.279415

5. Venugopal S, Mascarenhas J. The odyssey of pacritinib in myelofibrosis. 

. 2022;bloodadvances.2022007524. doi:10.1182/bloodadvances.2022007524

6. Chifotides HT, Bose P, Verstovsek S. Momelotinib: an emerging treatment for myelofibrosis patients with anemia. 

 2022;15(1):7. doi:10.1186/s13045-021-01157-4

7. Verstovsek S, Vannucchi A, Gerds A, et al. S195: MOMENTUM: phase 3 randomized study of momelotinib (MMB) versus danazol (DAN) in symptomatic and anemic myelofibrosis (MF) patients previously treated with a JAK inhibitor. 

. 2022;6:96-97. doi:10.1097/01.HS9.0000843672.56808.41

8. Verstovsek S, Chen CC, Egyed M, et al. MOMENTUM: momelotinib vs danazol in patients with myelofibrosis previously treated with JAKi who are symptomatic and anemic. 

. 2021;17(12):1449-1458. doi:10.2217/fon-2020-1048

9. Mesa R, Oh ST, Gerds AT, et al. Momelotinib reduces transfusion requirements in patients with myelofibrosis. 

. 2022;63(7):1718-1722. doi:10.1080/10428194.2022.2043304

10. Mesa R, Harrison C, Oh ST, et al. Overall survival in the SIMPLIFY-1 and SIMPLIFY-2 phase 3 trials of momelotinib in patients with myelofibrosis. 

 2022;10.1038/s41375-022-01637-7. doi:10.1038/s41375-022-01637-7

11. Venugopal S, Mascarenhas J. Novel therapeutics in myeloproliferative neoplasms. 

. 2020;13(1):162. doi:10.1186/s13045-020-00995-y

12. Chifotides HT, Bose P, Masarova L, Pemmaraju N, Verstovsek S. SOHO state of the art updates and next questions: novel therapies in development for myelofibrosis. 

. 2022;22(4):210-223. doi:10.1016/j.clml.2021.10.002

13. Newberry KJ, Patel K, Masarova L, et al. Clonal evolution and outcomes in myelofibrosis after ruxolitinib discontinuation. 

. 2017;130(9):1125-1131. doi:10.1182/blood-2017-05-783225

14. Bose P, Verstovsek S. SOHO state of the art updates and next questions: identifying and treating “progression” in myelofibrosis. 

. 2021;21(10):641-649. doi:10.1016/j.clml.2021.06.008

15. Shahin OA, Chifotides HT, Bose P, Masarova L, Verstovsek S. Accelerated phase of myeloproliferative neoplasms. 

. 2021;144(5):484-499. doi:10.1159/000512929

16. Mascarenhas JO, Verstovsek S. The clinical dilemma of JAK inhibitor failure in myelofibrosis: predictive characteristics and outcomes. 

. 2022;128(14):2717-2727. doi:10.1002/cncr.34222

17. Bose P, Verstovsek S. Management of myelofibrosis-related cytopenias. 

. 2018;13(3):164-172. doi:10.1007/s11899-018-0447-9

18. Vachhani P, Verstovsek S, Bose P. Disease modification in myelofibrosis: an elusive goal?. 

. 2022;40(11):1147-1154. doi:10.1200/JCO.21.02246

19. Gerds AT, Vannucchi AM, Passamonti F, et al. Duration of response to luspatercept in patients (Pts) requiring red blood cell (RBC) transfusions with myelofibrosis (MF) – Updated data from the phase 2 ACE-536-MF-001 study. 

 2020;136(Suppl 1):47-48. doi.10.1182/blood-2020-137265

20. Mascarenhas J, Gerds A, Verstovsek S. Paradigm shift: combination BET and JAK inhibition in myelofibrosis. 

. 2021;35(12):3361-3363. doi:10.1038/s41375-021-01405-z

21. Mascarenhas J, Kremyanskaya M, Patriarca A, et al. S198: BET inhibitor pelabresib (CPI-0610) combined with ruxolitinib in patients with myelofibrosis – JAK-inhibitor naïve or with suboptimal response to ruxolitinib – preliminary data from the MANIFEST study. 

2022;6:99-100. doi:10.1097/01.HS9.0000843684.97625.7e

22. Harrison C, Gupta V, Gerds AT, et al. Phase III MANIFEST-2: pelabresib + ruxolitinib vs. placebo + ruxolitinib in JAK-inhibitor treatment-naïve myelofibrosis. 

23. Passamonti F, Foran J, Tandra A, et al. S197: Navitoclax plus ruxolitinib in JAK-inhibitor naïve patients with myelofibrosis: preliminary safety and efficacy in a multicenter, open-label phase 2 study. 

 2022;6:98-99. doi:10.1097/01.HS9.0000843680.94912.c5

24. Harrison CN, Garcia JS, Somervaille TCP, et al. Addition of navitoclax to ongoing ruxolitinib therapy for patients with myelofibrosis with progression or suboptimal response: phase II safety and efficacy. 

. 2022;40(15):1671-1680. doi:10.1200/JCO.21.02188

25. Pemmaraju N, Garcia JS, Potluri J, et al. Addition of navitoclax to ongoing ruxolitinib treatment in patients with myelofibrosis (REFINE): a post-hoc analysis of molecular biomarkers in a phase 2 study. 

. 2022;9(6):e434-e444. doi:10.1016/S2352-3026(22)00116-8

26. Mascarenhas J, Komrokji RS, Palandri F, et al. Randomized, single-blind, multicenter phase II study of two doses of imetelstat in relapsed or refractory myelofibrosis. 

. 2021;39(26):2881-2892. doi:10.1200/JCO.20.02864

Articles

Srdan Verstovsek, MD, PhD, highlighted recent advancements in developing novel therapeutic strategies for myelofibrosis during SOHO 2022.

Novel Therapies in Development for Myelofibrosis Show Promise

Srdan Verstovsek, MD, PhD, a professor of Medicine and a hematologic oncologist at the University of Texas MD Anderson Cancer Center, discusses some of the best practices to try and prevent thrombosis in patients with polycythemia vera (PV).

Patients with PV can get thrombosis because the disease causes the patient’s bone marrow to make too many red blood cells. This then puts patients at risk for blood clots, which can cause other serious problems such as pulmonary embolisms.

Verstovsek highlights how clinicians need to watch patients’ hematocrit levels throughout their treatment and how the use of ruxolitinib (Jakafi) can potentially benefit these patients.

You want to, in either case, minimize the time the patients spend at about 45% hematocrit, because that increases the risk of blood clotting and the risk of dying. In the low-risk patients this is done by frequent phlebotomist, which means bloodletting. So low risk patients you phlebotomize and the patients and with that you would decrease the hematocrit. With phlebotomies, you also make people iron deficient. Iron is simply food for the red blood cells, and as more phlebotomies happen more iron deficiency happens, and that would decrease the rate of the phlebotomy. [However], there are patients that still require too many phlebotomies, maybe 3, 4, 5, or 6 [times] a year, so the bottom line is there are several patients that still spend a significant amount of time above 45% in their life. This is unnecessary.

In the high-risk group, we give patients, on top of phlebotomy, medications to eliminate the need for phlebotomy, because they're at higher risk for blood clotting. So we give them hydroxyurea 9 out of 10 times, which is a chemotherapy by mouth, [we also] sometimes give interferon injections, or we can even give them ruxolitinib, that would be a JAK2 inhibitor that is approved as a second line therapy. The goal here is to smooth that hematocrit percent below 45% all the time and eliminate a need for phlebotomy. That is not the case in every practice, there are many retrospective chart review studies that show that this is not achievable. And this is critical to maintain the patients below 45% all the time, particularly in the high-risk group. With the inability to control it we need new agents that would help maintain the hematocrit below 45% in high-risk group all the time. So, the need is there, either in the low risk group or in the high risk group to help achieve the goal of the therapy.

Srdan Verstovsek, MD, PhD, discusses some of the best practices to try and prevent thrombosis in patients with polycythemia vera.

Preventing Thrombosis in Patients with Polycythemia Vera

The phase 2 FIGHT-203 trial showed high rates of complete responses (CR) and complete cytogenetic responses in adult patients with relapsed or refractory myeloid/lymphoid neoplasms with 

 rearrangement, leading to the FDA approval of pemigatinib (Pemazyre).

In the multicenter, open-label, single-arm FIGHT-203 trial (NCT03011372), 18 out of 28 patients with chronic phase disease in the bone marrow with or without extramedullary disease (EMD) who were treated with pemigatinib achieved CR of 78% (95% CI; 52-94%). The median time to CR was 104 days (range, 44-435), and the median duration of CR was not reached (range, 1+ to 988+ days).

Among the 4 patients with blast phase disease in the bone marrow with or without EMD, 2 achieved CR with pemigatinib treatment. The duration of response ranged from 1 to 94 days. Of the 3 patients with EMD only, 1 patient achieved CR with a duration of 64+ days.

For all 28 patients enrolled in the study, the cytogenetic CR rate was 79% (95% CI, 59%-92%).

Regarding safety, the most common toxicities were hyperphosphatemia (74%), nail toxicity (62%), alopecia (59%), stomatitis (53%), diarrhea (50%), dry eye (50%), fatigue (44%), rash (35%), abdominal pain (35%), anemia (35%), constipation (32%), dry mouth (32%), epistaxis (29%), retinal pigment epithelial detachment (26%), extremity pain (26%), decreased appetite (24%), dry skin (24%), dyspepsia (24%), back pain (24%), nausea (21%), blurred vision (21%), peripheral edema (21%), and dizziness (21%). These adverse events occurred in more than 20% of the patients.

 rearrangement, the lack of effective therapies, or long-lasting effective therapies meant that the average survival was 1 year to 1 year and a half. Now having pemigatinib as a therapy transforms the outcome of these patients. It is an incredible development for these patients,” Verstovsek said,  in an interview with Targted Oncology

In the interview, Verstovsek discussed the FDA approval of pemigatinib, the FIGHT-203 trial, and possibilities for pemigatinib in the future.

TARGETED ONCOLOGY: Can you discuss myeloid/lymphoid neoplasms with 

 rearrangement? What treatment options were available for these patients before pemigatinib?

: For myeloid/lymphoid neoplasms that are driven by an abnormality in a gene called 

, the standard practice was to treat the patients with chemotherapy and see whether we could somehow get them to do the transplant. Otherwise, the chemotherapy, whether it was intensive chemotherapy in the hospital with intravenous medications, or oral chemotherapy- like hydroxyurea- was only used to control the disease. Even if we attempted to eliminate the disease with these interventions, the success rate was very low, and it only lasted for a few months at best.

 rearrangement, the lack of effective therapies, or long-lasting effective therapies meant that the average survival was 1 year to 1 year and a half. Now, having pemigatinib as a therapy transforms the outcome of the patients. It is an incredible development for these patients.

What background can you provide on the FIGHT-203 clinical trial?

A myeloid/lymphoid neoplasm with activation of gene 

 is a rather rare condition. Testing for presence of active 

 gene is not readily available. Individuals that have this disease, may present with myeloid disease like myeloproliferative neoplasm or acute myeloid leukemia or lymphoid disease like acute lymphoblastic leukemia or lymphoma. These are all possible presentations of this disease. These patients can be identified based on the analysis of chromosomes, however. When the bone marrow is obtained to diagnose any of these conditions, as a standard practice, we send a sample to a special lab to analyze whether there are any chromosomes that carry abnormalities. This is called karyotyping or cytogenetic testing. If the patients have abnormalities in chromosome 8p11, they are the ones that have activation of gene 

. This is easy way to identify them, if you can just remember that 8p11 chromosomal abnormality activates the 

It is not that common, but the marker that I described can help identify patients with 

 activation in everyday practice. Because we detected chromosomal abnormality in one of my own patients few years ago, we included that patient with 

 activation, in a clinical study and treated him with pemigatinib. That was a phase 1 study. He was one of many different types of patients with different diseases who responded to pemigatinib. He eliminated disease and that was unheard of. That led in part to the development of the phase 2 FIGHT-203 clinical study, which then led to approval of pemigatinib. Pemigatinib is now known to provide high level of clinical activity with about 80% of patients eliminating disease and that is testament to extraordinary transformational potential of the pemigatinib for these patients. Pemigatinib targets the FGFR1 protein that drives disease process.

This is how it started, with the identification of pemigatinib’s activity, realizing its potential, and with desire from an academic point of view and from the perspective of the company that produces pemigatinib, Incyte, to developed it. We all agreed that we cannot let this be forgotten. We engaged over several years to conduct FIGHT-203 study, to find those patients who had myeloid/lymphoid neoplasms with 

 rearrangement around the globe. I am so happy to see that this medication is approved.Now we have to go out and teach colleagues to look for patients with unusual clinical presentations that may have 8p11 chromosomal abnormality. It should become standard practice to look for the 8p11 Chromosomal abnormality, since these are the patients that are suitable patients for pemigatinib.

What do you think is next for pemigatinib?

Of course, this is not the first indication for this medication. It is valuable in some solid tumors. From my perspective as a leukemia doctor, I would envision that from now on we're going to combine pemigatinib with chemotherapy in some cases, for example when the patient presents with acute leukemia. In these cases the chemotherapy may be effective, but because of the aggressiveness of that condition, a combination of pemigatinib with chemotherapy may be even more effective. I would therefore expect the next wave of exploration of the utility of pemigatinib in malignant hematology to be in combination with other agents in patients that have complicated clinical picture with more aggressive clinical entities.

How do think this FDA approval has impacted the landscape?

I am just extraordinarily happy that in myeloproliferative neoplasms with 

 rearrangement, we have a new possibility for this small group of patients but with a very aggressive disease and be able to eliminate the disease in a high proportion of the patients. We can also potentially follow them longer and talk about the cure. This is not common at all in my field of myeloproliferative neoplasms.

1. Incyte announces FDA approval of Pemazyre® (pemigatinib) as the first and only targeted treatment for myeloid/lymphoid neoplasms (MLNs) with FGFR1 rearrangement. News release. Incyte. August 26, 2022. Accessed August 30, 2022. https://bwnews.pr/3wzSxxH

In the interview with Targeted Oncology, Srdan Verstovsek, MD, PhD, discussed the FDA approval of pemigatinib for relapsed or refractory myeloid/lymphoid neoplasms with FGFR1 rearrangement. He also discussed the FIGHT-203 trial, and possibilities for pemigatinib in the future.

Behind the FDA Approval: Pemigatinib for R/R Myeloid/Lymphoid Neoplasms

Srdan Verstovsek, MD, PhD, wraps up by discussing remaining unmet needs and hopes for future treatment options for patients with MF.