CTI BioPharma Research Articles

Impact of Symptom Benefit and Transfusion Response on Survival in Myelofibrosis Patients Treated with Pacritinib: PERSIST-2 Landmark Survival Analysis

Background: Pacritinib is a JAK1-sparing inhibitor of JAK2/IRAK1/ACVR1 that demonstrated symptom benefit measured by TSS (v2.0, excluding tiredness) vs best available therapy (BAT) in PERSIST-2, which enrolled cytopenic myelofibrosis patients with platelets ≤100×10 9/L. Recent datashowed that in patients with cytopenic MF, a ≥10% reduction in spleen volume at 12 weeks is associated with improved survival in patients treated with pacritinib ( Ajufo H, et al., J Clin Oncol;2023:14(16):Suppl). Surprisingly, this association was not confirmed in patients treated with BAT (82% of whom were on ruxolitinib). The association between other important measures of clinical benefit such as symptom burden reduction and anemia improvement on survival in patients treated with pacritinib has not previously been described. Methods: Patients randomized to pacritinib 200 mg BID and to BAT on PERSIST-2 were included if they were alive and on study at the start of the week 12 efficacy assessment period. Survival was assessed by Total Symptom Score (TSS; v2.0 excluding tiredness) reduction at various thresholds (≥50%, ≥20%, ≥10%, >0%) and transfusion independence (TI) response. TI was assessed among patients who required red blood cell (RBC) transfusion at baseline (within 90 days) and was defined, for the purposes of a landmark survival analysis, as the absence of RBC transfusions over any 12-week period from first dose through week 14 (allowing for a ±2-week window around week 12). Overall survival (OS) was estimated via the K-M method following the landmark approach; survival in responders vs non-responders was compared using the log-rank test. Results: Of the 59 patients treated with pacritinib who had a reduction of TSS≥10%, the median age was 67 years, 25% had a baseline high-risk DIPSS, median platelet count was 61 x10 9/L, median hemoglobin was 9.7 g/dL, and baseline TSS was 19.1. Reduction of TSS≥10% was associated with improved OS, with 1 death among 59 responders vs 4 deaths among 30 non-responders (hazard ratio [HR]=0.12, 95% confidence interval [CI]: 0.01, 0.79] P=0.021, Fig 1a). Similar to spleen volume reduction, the association between TSS response and OS weakened at more stringent TSS response thresholds (Fig 1c, e), with the BAT arm not showing an association between TSS response and OS at any threshold. (Fig 1b, d, f). In order to assess the relationship of specific TSS domains and survival , a landmark OS analysis was performed based on ≥20% reduction in physical function scores (sum of ‘tiredness’ and 'inactivity'), spleen-related symptom scores (sum of 'abdominal discomfort', ‘early satiety’, and 'left rib pain'), and cytokine-related symptom scores (sum of 'itching', ‘night sweats’, and ‘bone pain‘). For cytokine-related symptoms, the number of deaths in PAC responders was significantly different compared to non-responders, with 0 deaths among 35 responders vs 2 among 15 non-responders ( P=0.0325). Conversely the deaths among responders (2/22) vs non-responders (2/20) were not significantly different in the BAT arm. For the physical function and spleen-related symptom subscales, no significant differences between PAC responders and non-responders was observed (HR=0.60; 95% CI [0.05, 6.74] P=0.679) and (HR=0.26; 95% CI 0.02, 2.93, P=0.2435) respectively. Among 36 patients on PAC who received RBC transfusions at baseline, 7 achieved TI over at least a 12-week period up to the time of the landmark analysis. There were no deaths among TI responders compared to 2 (6.9%) among TI non-responders. There were too few TI responders on BAT (only 2 out of 38) to assess the impact on survival. Conclusion: In cytopenic myelofibrosis patients enrolled in PERSIST-2, having a reduction of TSS≥10% on full-dose PAC was associated with OS benefit - a finding that has not been noted with other JAK inhibitors to date. By contrast, this association was not found with BAT, (82% of these patients received ruxolitinib). Thus, reductions in TSS in patients treated with PAC were associated with an OS benefit. It is possible that pacritinib, with its distinctive mechanism of action, may offer a unique survival advantage for MF patients with moderate or severe thrombocytopenia, and further studies are required to understand the potential mechanisms of these distinct clinical observations. Study funded by CTI BioPharma Corp., a Sobi company.

An Analysis of Ruxolitinib Dosing for Myelofibrosis in Real-World Practice

Background: Myelofibrosis (MF) is a myeloid neoplasm characterized by splenomegaly, constitutional symptoms, and cytopenias. Notably, worsening cytopenias in MF patients is directly correlated with poor survival ( Coltro, et al. Blood Cancer J. 2022;12(8):116). The JAK1/2 inhibitor ruxolitinib (RUX) is effective in decreasing splenomegaly and improving symptom control at starting doses of 30-40 mg total daily dose (TDD), though drug-induced cytopenias often lead to significant dose reductions. Doses of ≤20 mg TDD are associated with decreased efficacy for spleen response, and doses of ≤10 mg TDD demonstrate minimal efficacy for spleen or symptom reduction ( Verstovsek, et al. Onco Targets Ther. 2014;7:13-21). Treating with less clinically effective doses may not be optimal in light of newer, less myelosuppressive JAK2 inhibitors that can be administered without dose reduction, regardless of baseline cytopenias. This study describes RUX dosing patterns in real-world community practice. Methods: This retrospective, observational study included deidentified data of adult patients from the IntegraConnect PrecisionQ database (~80% community practice) with MF treated with first-line RUX and with ≥2 office visits (with a criterion of 2 MF diagnosis codes reported within 180 days) from January 2016 to July 2022. Patients were stratified by baseline platelet count (PLT). Data on RUX TDD at initiation and at first dose modification were collected, with a focus on less clinically effective dosing of ≤20 mg TDD and ≤10 mg TDD. Results: Of 129 patients on RUX with a median age of 75 (range: 42-89) years, 61% (n=79) had PLT >200x10 9/L, 19% (n=24) had PLT 100-200x10 9/L, and 20% (n=26) had PLT <100x10 9/L. Across all PLT strata, 88% (n=114) were initiated on RUX at a TDD of ≤20 mg, and 51% (n=66) were started at a TDD ≤10 mg. Nearly half of patients with higher baseline platelet counts (>100 x 10 9/L) were started on doses ≤10 mg TDD (Fig 1). Among 79 patients with PLT >200x10 9/L, starting RUX TDD was ≤20 mg in 87% (n=69) and ≤10 mg in 43% (n=34). A total of 49 patients underwent subsequent dose modification (median time [min, max]: 47 days [10, 1336], with 19 dose increases vs 30 dose decreases. Of patients whose dose increased, only 4 escalated to a TDD >20 mg. Despite dose modification, RUX TDD remained ≤20 mg in 90% (44/49) and ≤10 mg in 43% (21/49) of patients. Similar to patients with baseline PLT >200x10 9/L, the majority of patients with PLT 100-200x10 9/L started on TDD ≤20 mg (87.5% [21/24]), with a high proportion on ≤10 mg (50% [12/24]). Among the 103 patients with PLT >100x10 9/L for whom a recommended starting dose is provided in the RUX package insert, 88% (91/103) initiated RUX below the recommended dose. Of the 61 patients who underwent subsequent dose modification (median time: 47 days [10, 1336], only 10% (6/61) were escalated to a dose recognized as clinically effective. Conclusions: These real-world data suggest that a majority of patients starting RUX, including those with PLT >200x10 9/L, are initiated on ≤20 mg TDD, and the majority of patients are not titrated up to the doses tested in the pivotal studies that led to RUX approval. These data suggest that clinicians are hesitant to prescribe RUX at doses known to be clinically effective. Together with the timing of dose modification, this suggests that there may be concerns related to toxicity or treatment-related cytopenias. Recognizing that JAK2 inhibition remains an important part of managing MF for patients, clinicians now have alternative treatment options. These newer treatments inhibit additional pathways (IRAK1/ACVR1), are less myelosuppressive, and can maintain dose intensity regardless of baseline platelet count. Study funded by CTI BioPharma Corp., a Sobi Company.

Retrospective Analysis of the Relationship between Transfusion Independence and Bone Marrow Fibrosis Reduction in Patients with Myelofibrosis Treated with Pacritinib Versus Ruxolitinib

Background Pacritinib is a JAK1-sparing JAK2/IRAK1/ACVR1 inhibitor for treatment of myelofibrosis (MF). In addition to improving spleen volume and symptoms, pacritinib is associated with anemia benefit in MF patients. Recent in vivo studies have shown that dual JAK2/IRAK1 inhibition is associated with improvement in both cytopenias and bone marrow reticulin fibrosis (BMF) in an inflammation-driven murine MF model ( Cuenca Zamora E, et al. EHA 2023; P987 and P990). Here, we retrospectively analyzed the relationship between achieving transfusion independence and reduction in BMF in MF patients treated with pacritinib 200 mg twice daily (BID) vs ruxolitinib (RUX) on the phase 3 PERSIST-2 study. Methods: PERSIST-2 enrolled patients with platelet counts ≤100 x 10 9/L. This analysis focused on pacritinib 200 mg BID and on patients who received RUX as best available therapy (BAT) who enrolled ≥12 weeks prior to study termination and who required red blood cell (RBC) transfusions at baseline. The proportion of patients who achieved transfusion independence response (TI-R, any 12-week interval with no RBC transfusions) was ascertained for pacritinib vs RUX. The proportion of patients with BMF reduction (≥1 grade decrease in reticulin fibrosis from baseline at week 24) was reported among patients on pacritinib achieving TI-R vs. non-response (NR). Results: The analysis included 41 patients on pacritinib (median dose intensity 100% through week 24) and 18 on RUX (median daily dose 10mg at week 24). Baseline characteristics were similar between the groups, including median platelet count (41 vs 38 x 10 9/L) and median hemoglobin (8.7 vs 8.6 g/dL). All patients required RBC transfusion at baseline. A significantly greater proportion of patients treated with pacritinib vs RUX achieved TI through week 24: 37% (n=15/41) vs 6% (n=1/18), P=0.023. Nominally, this trend held for those with baseline platelets <50 x 10 9/L: 28% vs 8%, P=0.222. In addition, a greater percentage achieved a 50% reduction in RBC transfusions over any 12 weeks (49% vs 6%, P=0.001). Paired bone marrow assessments at baseline and week 24 were available for 18/41 of patients on pacritinib, of whom 44% (8/18) achieved TI-R on study. The proportion of patients who experienced BMF reduction (>=1 grade at any point) was significantly greater among TI-R (62.5%, n=5/8) compared to TI-NR (10%, n=1/10) on pacritinib ( P=0.043). Of the 5 patients who achieved TI-R and BMF reduction, all had grade 2-3 fibrosis at baseline, and 2 experienced a reduction from grade 3 to grade 1 ( Figure 1). By contrast, paired bone marrow biopsies were available for 5 patients on RUX, and there was no association between fibrosis reduction in TI-R (0%, n=0/1) and TI-NR (25%, n=1/4). Conclusions: In cytopenic MF patients from PERSIST-2, TI-R on pacritinib was associated with BMF improvement. Though these results are based on a small sample size, they contrast with recent data suggesting no correlation between BMF reduction and TI-R on the JAK1/2 inhibitors momelotinib and ruxolitinib ( Oh ST, et al. Blood 2022;140 (Supp 1):821-23). While differences in study design could have impacted these results, these findings suggest that distinct inhibitory profiles may further distinguish the clinical impact of these treatments. Further studies are warranted to confirm the relationship between BMF reduction and anemia benefit in patients treated with pacritinib. Study funded by CTI BioPharma Corp., a Sobi company

Platelet Response in Pacritinib-Treated Patients with Cytopenic Myelofibrosis: A Retrospective Analysis of PERSIST-2 and PAC203 Studies

Background: Myelofibrosis (MF) is a myeloid malignancy characterized by clonal hematopoisis, bone marrow fibrosis (BMF) and ineffective extramedullary hematopoiesis, resulting in progressive cytopenias. Thrombocytopenia is both prognostic of poor outcomes and predictive of treatment intolerance with the JAK1/2 inhibitor ruxolitinib, which exacerbates cytopenias. Pacritinib is a JAK1-sparing inhibitor of JAK2/IRAK1/ACVR1 that can be administered at full dose to patients regardless of baseline platelet count (PLT). While prior studies have shown that pacritinib is associated with PLT stability in most patients, PLT improvement has not been described outside of a recently published case report ( Yacoub A, et al. JCO Precis Oncol. 2023;7:e2200523). Here, we report rates of hematologic improvement in PLTs (HI-P) with pacritinib across two clinical trials. Methods: Patients with baseline PLT ≤100x10 9/L on the pacritinib 200 mg BID arms of the phase 3 PERSIST-2 study (randomized ≥12 weeks prior to study termination) or the phase 2 dose-finding PAC203 study were included. HI-P was defined per International Working Group (IWG) criteria (baseline PLT <20x10 9/L: increase to >20x10 9/L and by at least 100%; baseline PLT 20-100 x 10 9/L: absolute increase of ≥30x10 9/L) in the absence of PLT transfusions, sustained over any 8 weeks while on treatment. Efficacy outcomes (reduction in spleen volume, symptom score, and BMF) were compared between HI-P responders vs non-responders (those who did not meet IWG criteria). Rates of PLT improvement were also analyzed on the best available therapy (BAT) arm of the PERSIST-2 study over the treatment period (end of study treatment). Results: Of 117 patients randomized to pacritinib (75 from PERSIST-2, 42 from PAC203), 16% (n=19) experienced HI-P on study (as defined in methods). Additionally, 14 of the 19 HI-P patients had sustained platelet improvement over ≥12 weeks). By contrast, only 5% (4/77) of patients on BAT achieved HI-P response prior to end of study treatment. HI-P responders on pacritinib compared to non-responders, had numerically higher median baseline PLT count (63 vs 45x10 9/L) and hemoglobin (Hb; 10.3 vs 8.8 g/dL). A similar percentage had prior (<30 days) JAK2 inhibitor exposure (68.4% vs 66.3%) and JAK2V617F mutation (78.9 vs 74.5%); median JAK2 allele burden was low in both responders and non-responders (26.7% vs 36.9%). Among HI-P responders with prior ruxolitinib exposure, most (85%, 11/13) had recent exposure within the prior 30 days, with median dose of 10 mg BID. PLT improvement was noted within the first 12 weeks in most HI-P responders, whereas PLT count remained stable, on average, among non-responders ( Figure 1a). To evaluate if recent ruxolitinib exposure and washout of drug was responsible for HI-P, we analyzed the subset of patients with ruxolitinib exposure in previous 30 days (11/19). The mean platelet count increased from 56 to 141x10 9/L at week 12. In the remaining 8/19 patients without recent ruxolitinib exposure (n=6 were treatment naïve), platelets increased from 59 to 102 x 10 9/L at week 12. While there was no difference in the magnitude of spleen volume or symptom score reduction in HI-P responders vs non-responders, a correlation with change in BMF was noted. Among the 36 patients with available bone marrow data from baseline and week 24, HI-P responders were numerically more likely to have BMF reduction (67%, n=4/6) compared to non-responders (23%, n=7/30, P=0.057, Figure 1b). There was no difference in the rate of hemorrhagic events (by standardized MedDRA queries) in PLT responders vs non-responders (47% vs 46%), though grade ≥3 bleeding was observed at lower frequency in responders compared to non-responders (10.5% vs 16%). Other commonly reported adverse events with pacritinib occurred at similar frequency between responders and non-responders. Discussion: PLT improvement meeting IWG criteria occurs in a subset of MF patients treated with pacritinib and does not seem to be explained by changes in spleen volume. Further studies are warranted to assess the correlation between hematologic improvement and BMF reduction with pacritinib. It is possible that pacritinib's unique mechanism of action as an IRAK1 inhibitor could result in modulation of the bone marrow microenvironment and thrombopoiesis. Study funded by CTI BioPharma Corp., a Sobi company.

(173) Integration of an Adjunct E-health Biopsychosocial Platform into a Multi-disciplinary Sexual Health Clinic at a Prostate Cancer Survivorship Program

Abstract Introduction The Sexual Health Clinic (SHC) in a prostate cancer survivorship program uses a biopsychosocial approach for prostate cancer (PCa) survivors and their partners. SHAReClinic (SHARe) is a web-based biopsychosocial platform developed with funding from Movember to help PCa survivors and their partners adapt to and recover sexual function after PCa treatment. The SHC implemented the SHARe program as an adjunct therapy and resource in Nov 2021 for patients participating in the SHC in-person/virtual appointments. Objective To evaluate demographics and value of an adjunct e-health biopsychosocial platform within an established multi-disciplinary SHC between Nov 2021 and Jun 2022. Methods Patients enrolling in the SHC are introduced to SHARe at the pre-clinic education session. SHARe enrollment is recommended but not mandatory. Patients receive up to 3 verbal or email reminders from the clinician and program staff to sign up on-line for SHARe. SHC-SHARe patients were matched with SHC patients who did not register for the SHARe by i) the time from treatment to the first appointment at SHC, ii) age at diagnosis and age when invited to participate in the survey. Responses were collected over the same time period of 6 days. Mann-Whitney tests were conducted to compare the two groups. Results Between Nov 8, 2021 and Jun 23, 2022, 94 new patients were seen. 58/94 patients were interested and received a code for on-line registration for SHARe, but only 24/58 (41%) activated their code. Median time from receiving the code to activation is 6.5 (0-109) days. 24 SHC only patients were matched to the SHC-SHARe patients by the criteria listed above. We observed a higher proportion of the SHC-SHARe patients to be caucasian (75% vs 50%) and retired (63% vs 42%) compared to the matched group (Table 1). 12/24 (50%) SHC-SHARe patients responded to the survey. 11/12 (92%) agreed with the statement that SHARe was helpful in reinforcing the material learning in the clinic. 8/24 (33%) SHC pts responded to the survey. Technical issues, forgetting to sign up, and not being interested were reasons cited by patients for not participating in SHARe. 2/8 (25%) respondents thought they had signed up for SHARe. No significant differences were found between the score for the overall experience with the SHC, how helpful the clinic was, or the likelihood to refer others to the clinic. Conclusions Overall, the integration of SHARe as an adjunct resource into the SHC was successful. Lack of other languages available on SHARe may a barrier for non-Native English speakers. While patient satisfaction did not differ between groups, 92% of SHC-SHARe patients agreed that the e-learning platform was helpful in reinforcing the material taught in the clinic. Although our sample size is small, it is clear that the addition of SHARe to our SHC is beneficial. We are exploring strategies to improve the registration rate to SHARe for the 59% who were interested but did not use the registration code. Disclosure Any of the authors act as a consultant, employee or shareholder of an industry for: Dr. Flannigan - Boston Scientific, Coloplast, Sustained Therapeutics; Dr. Higano - Consulting fees or honoraria: AstraZeneca Astellas Genetech Lantheus Merck Sharp & Dohme Myovant Menarini Tolmar Vaccitech Verity, Stock ownership: CTI Biopharma, Expert testimony: Ferring.

MPN-141 Retrospective Comparison of Patient Outcomes on Pacritinib Versus Ruxolitinib in Patients With Myelofibrosis and Thrombocytopenia.

Pacritinib (PAC) is a JAK2/IRAK1 inhibitor for patients with myelofibrosis (MF) and thrombocytopenia. Unlike the JAK1/2 inhibitor ruxolitinib (RUX), which is used at lower doses in patients with thrombocytopenia, PAC has been studied at full dose regardless of platelet count. This analysis focused on PERSIST-2 patients with platelet counts ≤100 × 109/L who were randomized to PAC 200mg BID and patients who received RUX on best available therapy (BAT) prior to week 24. Endpoints included percent of patients with 35% spleen volume reduction (SVR), 50% modified total symptom score (mTSS) reduction (based on early satiety, abdominal discomfort, night sweats, itching, bone pain, and rib pain), and improvement in disease symptoms measured by Patient Global Impression of Change (PGIC). Safety analyses were based on all treated patients; efficacy analyses were based on the intention-to-treat population randomized at least 22 weeks prior to study end. The Fisher Exact test was used to describe differences in response. Logistic and Cox regression was used to adjust for differences in baseline characteristics. Safety analysis included 106 patients on PAC and 44 on RUX; efficacy analysis included 74 on PAC and 32 on RUX (median total daily dose 10 mg). Baseline characteristics were similar between groups, including median platelet count (55 vs 61 × 109/L) and percent receiving RBC transfusion (46% vs 43%). Patients treated with PAC vs RUX achieved higher rates of SVR (22% vs 3%, p=0.02) and numerically higher rates of mTSS response (35% vs 19%; p=0.11) and "much" or "very much" improved symptoms (35% vs 16%, p=0.06) at week 24. Among RUX patients with an available PGIC measure at week 24, 50% reported either no improvement or worsening symptoms, while 76% of PAC patients reported improvement. The adjusted hazard ratio on PAC vs RUX was 0.46 [95% CI: 0.15-1.43]. Bleeding occurred at similar rates (43% vs 41%) on PAC vs RUX. Fatal AEs occurred in 8% on PAC compared to 11% on RUX. PAC yielded higher response rates and a similar safety profile to lower-dose RUX in patients with MF who have moderate or severe thrombocytopenia. This study was supported by CTI BioPharma.

European LeukemiaNet Response Predicts Disease Progression but Not Thrombosis in Polycythemia Vera.

European LeukemiaNet Response Predicts Disease Progression but Not Thrombosis in Polycythemia Vera.

Pacritinib: First Approval

Pacritinib (VONJO™) is an orally administered, small molecule kinase inhibitor being developed by CTI BioPharma for the treatment of myelofibrosis and graft-versus-host disease. Pacritinib received its first approval in February 2022 in the USA for the treatment of adults with intermediate- or high-risk primary or secondary (post-polycythemia vera or post-essential thrombocythemia) myelofibrosis with a platelet count below 50 × 109/L. The accelerated approval was based on results from the randomized, active-controlled, phase III PERSIST-2 trial, in which spleen volume reduction was demonstrated in pacritinib recipients. This article summarizes the milestones in the development of pacritinib leading to this first approval for myelofibrosis.

Venetoclax and hypomethylating agents in older/unfit patients with blastic plasmacytoid dendritic cell neoplasm

Venetoclax and hypomethylating agents in older/unfit patients with blastic plasmacytoid dendritic cell neoplasm

The Impact of Pacritinib on Myelofibrosis Symptoms in Patients with Moderate and Severe Thrombocytopenia: A Retrospective Analysis of Patients in the Persist-2 Study

The Impact of Pacritinib on Myelofibrosis Symptoms in Patients with Moderate and Severe Thrombocytopenia: A Retrospective Analysis of Patients in the Persist-2 Study

A Retrospective Head-to-Head Comparison between Pacritinib and Ruxolitinib in Patients with Myelofibrosis and Moderate to Severe Thrombocytopenia

A Retrospective Head-to-Head Comparison between Pacritinib and Ruxolitinib in Patients with Myelofibrosis and Moderate to Severe Thrombocytopenia

Subgroup Analysis from a Phase 2 Study of the Efficacy and Safety of Parsaclisib, a Selective PI3Kδ Inhibitor, in Combination with Ruxolitinib in Patients with Myelofibrosis (MF)

Subgroup Analysis from a Phase 2 Study of the Efficacy and Safety of Parsaclisib, a Selective PI3Kδ Inhibitor, in Combination with Ruxolitinib in Patients with Myelofibrosis (MF)

Safety and Tolerability of Fedratinib (FEDR), an Oral Inhibitor of Janus Kinase 2 (JAK2), in Patients with Intermediate- or High-Risk Myelofibrosis (MF) Previously Treated with Ruxolitinib (RUX): Results from the Phase 3b FREEDOM Trial

Safety and Tolerability of Fedratinib (FEDR), an Oral Inhibitor of Janus Kinase 2 (JAK2), in Patients with Intermediate- or High-Risk Myelofibrosis (MF) Previously Treated with Ruxolitinib (RUX): Results from the Phase 3b FREEDOM Trial

Pelabresib (CPI-0610) Monotherapy in Patients with Myelofibrosis - Update of Clinical and Translational Data from the Ongoing Manifest Trial

Pelabresib (CPI-0610) Monotherapy in Patients with Myelofibrosis - Update of Clinical and Translational Data from the Ongoing Manifest Trial

A Phase 1/2 Study of Single Agent Tagraxofusp, a First-in-Class CD123-Targeted Therapy, in Patients with Myelofibrosis That Is Relapsed/Refractory Following JAK Inhibitor Therapy

A Phase 1/2 Study of Single Agent Tagraxofusp, a First-in-Class CD123-Targeted Therapy, in Patients with Myelofibrosis That Is Relapsed/Refractory Following JAK Inhibitor Therapy

Disease-Modifying Potential of BET Inhibitor Pelabresib (CPI-0610) As Demonstrated By Improvements in Bone Marrow Function and Clinical Activity in Patients with Myelofibrosis - Preliminary Data

Disease-Modifying Potential of BET Inhibitor Pelabresib (CPI-0610) As Demonstrated By Improvements in Bone Marrow Function and Clinical Activity in Patients with Myelofibrosis - Preliminary Data

Evidence of NF-ΚB Pathway Activation in Patients with Advanced, High Molecular Risk Myelofibrosis

Evidence of NF-ΚB Pathway Activation in Patients with Advanced, High Molecular Risk Myelofibrosis

Integrated Safety Analysis of Tagraxofusp, a CD123-Directed Targeted Therapy, in Patients with Hematologic Malignancies

Integrated Safety Analysis of Tagraxofusp, a CD123-Directed Targeted Therapy, in Patients with Hematologic Malignancies

Treatment of Myelofibrosis Patients with the TGF-β 1/3 Inhibitor AVID200 (MPN-RC 118) Induces a Profound Effect on Platelet Production

Treatment of Myelofibrosis Patients with the TGF-β 1/3 Inhibitor AVID200 (MPN-RC 118) Induces a Profound Effect on Platelet Production

Tagraxofusp (SL-401) in Patients with Chronic Myelomonocytic Leukemia (CMML): Updated Results of an Ongoing Phase 1/2 Trial

Tagraxofusp (SL-401) in Patients with Chronic Myelomonocytic Leukemia (CMML): Updated Results of an Ongoing Phase 1/2 Trial