PracticeVideosBlogFlashcardsEspañol

Free exam prep

BCOP Board Certified Oncology Pharmacist

Practice QuestionsStudy Guide

11.2 Chronic Leukemias & Myeloproliferative Neoplasms

Key Takeaways

  • Chronic Myeloid Leukemia (CML) is driven by the BCR::ABL1 fusion oncoprotein t(9;22); frontline TKI selection balances efficacy and toxicity (imatinib for low risk; dasatinib for pleural effusion vigilance and strict PPI avoidance; nilotinib with fasting requirements and cardiovascular/QTc monitoring; bosutinib with GI management; and asciminib/ponatinib for refractory disease or the T315I gatekeeper mutation).
  • CML molecular response milestones on the International Scale (IS) dictate therapeutic milestones: BCR::ABL1 <=10% at 3 and 6 months, <=0.1% (Major Molecular Response, MMR/MR3) at 12 months, and deep sustained response (MR4/MR4.5 for >=2 years on TKI >=3-5 years) to qualify for Treatment-Free Remission (TFR) trials.
  • Chronic Lymphocytic Leukemia (CLL) treatment is guided by TP53 mutation / del(17p) and IGHV mutational status; frontline standards are chemotherapy-free, utilizing continuous second-generation BTK inhibitors (acalabrutinib, zanubrutinib) or fixed-duration venetoclax + obinutuzumab (12 months per CLL14) with mandatory 5-week venetoclax TLS ramp-up.
  • The T315I BCR::ABL1 mutation confers pan-resistance to imatinib, dasatinib, nilotinib, and bosutinib, remaining sensitive ONLY to ponatinib (45 mg daily de-escalated to 15 mg upon response to mitigate arterial occlusive events) and the allosteric STAMP inhibitor asciminib (200 mg BID).
  • Myeloproliferative Neoplasms (PV, ET, Myelofibrosis) driven by JAK2/CALR/MPL mutations require risk-directed management: PV mandates strict Hematocrit <45% control (CYTO-PV); Myelofibrosis leverages JAK inhibitors tailored to comorbidities—ruxolitinib for splenomegaly, fedratinib with mandatory thiamine monitoring for Wernicke encephalopathy, pacritinib for severe thrombocytopenia (platelets <50k), and momelotinib for anemia.
Last updated: August 2026

11.2 Chronic Leukemias & Myeloproliferative Neoplasms

Chronic hematologic malignancies encompass a spectrum of indolent to progressive clonal stem cell disorders. Unlike acute leukemias characterized by differentiation arrest, chronic leukemias and myeloproliferative neoplasms (MPNs) demonstrate persistent proliferation and accumulation of mature, functional or semi-functional myeloid and lymphoid elements.

Modern management in this domain relies heavily on oral targeted small-molecule kinase inhibitors (BCR::ABL1, BTK, BCL-2, JAK1/2, ACVR1 inhibitors). Board-certified oncology pharmacists must navigate nuanced drug-drug interactions, long-term cardiovascular and metabolic safety profiles, molecular monitoring milestones, and biomarker-guided resistance algorithms.

1. Chronic Myeloid Leukemia (CML): Pathophysiology & TKI Therapeutics

CML is a clonal myeloproliferative neoplasm characterized by the reciprocal chromosomal translocation t(9;22)(q34.1;q11.2), creating the Philadelphia Chromosome (Ph). This juxtaposition fuses the Abelson murine leukemia viral oncogene homolog 1 (ABL1) on chromosome 9 to the breakpoint cluster region (BCR) on chromosome 22, generating the constitutively active BCR::ABL1 tyrosine kinase oncoprotein that drives downstream JAK/STAT, PI3K/AKT, and RAS/MAPK signaling.

+-----------------------------------------------------------------------------+
|                   CML TYROSINE KINASE INHIBITOR (TKI) MASTER MATRIX         |
+-----------------------------------------------------------------------------+
| 1. IMATINIB (Gleevec) - 1st Generation                                      |
|    - Dose: 400 mg PO daily WITH A MEAL and large glass of water (reduces GI)|
|    - Signature Toxicities: Fluid retention / periorbital edema, muscle      |
|      cramps, nausea, diarrhea, fatigue, mild myelosuppression.              |
|    - Resistance: Ineffective against T315I, F317L, Y253H mutations.         |
|-----------------------------------------------------------------------------|
| 2. DASATINIB (Sprycel) - 2nd Generation (325x more potent than imatinib)    |
|    - Dose: 100 mg PO daily (with or without food)                           |
|    - Signature Toxicities: **Pleural / Pericardial Effusions (20-30%)**,    |
|      **Pulmonary Arterial Hypertension (PAH)**, platelet dysfunction/bleeding|
|    - CRITICAL PHARMACY INTERACTION: **Requires gastric acid for solubility**|
|      * Proton Pump Inhibitors (PPIs): STRICTLY CONTRAINDICATED / AVOID      |
|      * H2-Receptor Antagonists: Take dasatinib 2 hr before or 10 hr after H2RA|
|      * Antacids: Separate by at least 2 hours                               |
|-----------------------------------------------------------------------------|
| 3. NILOTINIB (Tasigna) - 2nd Generation (30x more potent than imatinib)     |
|    - Dose: 300 mg PO BID (frontline) or 400 mg PO BID (resistant)           |
|    - STRICT ADMINISTRATION MANDATE: **TAKE ON AN EMPTY STOMACH**            |
|      * Food increases absorption dramatically, increasing fatal toxicity!   |
|      * Fast 2 hours before and 1 hour after dose                            |
|    - Black Box Warnings: **QTc Prolongation & Sudden Death**, **Arterial    |
|      Occlusive Events (Peripheral Arterial Disease, Stroke, MI)**           |
|    - Metabolic Toxicities: Hyperglycemia, Hypercholesterolemia, Pancreatitis|
|-----------------------------------------------------------------------------|
| 4. BOSUTINIB (Bosulif) - 2nd Generation (Dual Src/Abl inhibitor)            |
|    - Dose: 400 mg PO daily WITH FOOD (frontline) or 500 mg PO daily         |
|    - Signature Toxicities: **Severe Early Diarrhea (70-80%)**, Nausea,      |
|      Transaminitis. Manage diarrhea aggressively with loperamide.           |
|-----------------------------------------------------------------------------|
| 5. PONATINIB (Iclusig) - 3rd Generation (Active against T315I Mutation)     |
|    - Dose: 45 mg PO daily (de-escalate to 15 mg daily upon achieving MCyR)  |
|    - Black Box Warnings: **Severe Arterial Occlusive Events (AOEs: 25-35%)**|
|      (Myocardial infarction, ischemic stroke, severe peripheral ischemia),  |
|      Venous thromboembolism, Heart Failure, Hepatotoxicity, Pancreatitis    |
|-----------------------------------------------------------------------------|
| 6. ASCIMINIB (Scemblix) - STAMP Inhibitor (Allosteric ABL Pocket Binder)    |
|    - Mechanism: Specifically Targets the ABL Myristoyl Pocket (STAMP)       |
|    - Dose: 40 mg PO BID or 80 mg daily (resistant CP-CML) on EMPTY STOMACH  |
|      **200 mg PO BID** for **T315I mutation** (overcomes ATP-site resistance)|
|    - Signature Toxicities: Musculoskeletal pain, fatigue, lipase elevation  |
+-----------------------------------------------------------------------------+

Molecular Monitoring & Treatment-Free Remission (TFR)

Quantitative Real-Time PCR (qPCR) measuring BCR::ABL1 transcript levels standardized to the International Scale (IS) dictates clinical decision-making:

+-----------------------------------------------------------------------------+
|            BCR::ABL1 (IS) MILESTONES & THERAPEUTIC MILESTONE GATING         |
|                                                                             |
|   - **3 Months:**  *BCR::ABL1* <= 10% (Early Molecular Response [EMR])      |
|   - **6 Months:**  *BCR::ABL1* <= 10% (Red flag if > 10% -> check adherence/|
|                    mutations / switch TKI)                                  |
|   - **12 Months:** *BCR::ABL1* <= 0.1% (**Major Molecular Response: MMR /   |
|                    MR3.0** [3-log reduction])                               |
|   - **Deep Molecular Response (DMR):**                                      |
|     * **MR4.0:**   *BCR::ABL1* <= 0.01% (4-log reduction)                   |
|     * **MR4.5:**   *BCR::ABL1* <= 0.0032% (4.5-log reduction)               |
|                                                                             |
|   [TREATMENT-FREE REMISSION (TFR) CRITERIA]                                 |
|   1. Chronic phase CML on approved TKI for >= 3 to 5 years                  |
|   2. Sustained Deep Molecular Response (>= MR4.0 or MR4.5) for >= 2 years   |
|   3. Access to certified, rapid qPCR testing (results within 4 weeks)       |
|   4. Monthly qPCR monitoring for the first 12 months after TKI cessation    |
|   5. Immediate TKI resumption if loss of MMR (*BCR::ABL1* > 0.1% IS)        |
+-----------------------------------------------------------------------------+

+-----------------------------------------------------------------------------+
|               CML T315I "GATEKEEPER" MUTATION ALGORITHM                     |
|                                                                             |
|   Identification of *BCR::ABL1* T315I Mutation (Threonine to Isoleucine 315)|
|   - Sterically hinders the ATP-binding pocket                               |
|   - Confers PAN-RESISTANCE to: Imatinib, Dasatinib, Nilotinib, Bosutinib    |
|                                                                             |
|   ACTIONABLE THERAPEUTIC OPTIONS:                                           |
|   1. **Ponatinib:** 45 mg PO daily -> de-escalate to 15 mg upon response    |
|   2. **Asciminib:** 200 mg PO twice daily on an empty stomach               |
|   3. **Allogeneic Stem Cell Transplantation** in eligible candidates        |
+-----------------------------------------------------------------------------+

2. Chronic Lymphocytic Leukemia (CLL): Biomarkers & Modern Paradigms

CLL is a clonal malignancy of mature, CD5+/CD19+/CD23+ B lymphocytes. Initiation of therapy is restricted to patients with active, symptomatic disease meeting International Workshop on CLL (iwCLL) criteria (progressive marrow failure, massive/symptomatic splenomegaly or lymphadenopathy, lymphocyte doubling time < 6 months, or constitutional B-symptoms).

+-----------------------------------------------------------------------------+
|                  CLL PROGNOSTIC BIOMARKER STRATIFICATION                   |
|                                                                             |
|   [TP53 MUTATION / DEL(17p)] (Highest Risk)                                 |
|   - Loss of tumor suppressor p53 causes chemoimmunotherapy resistance (FCR/ |
|     BR are strictly contraindicated!).                                      |
|   - Mandates TARGETED THERAPY: BTK Inhibitors (Zanubrutinib/Acalabrutinib)  |
|     or Venetoclax-based regimens.                                           |
|                                                                             |
|   [IGHV MUTATIONAL STATUS]                                                  |
|   - **Unmutated IGHV (>=98% homology):** Aggressive disease arising from    |
|     pre-germinal center B cells; poor response to chemo; excellent with TKIs|
|   - **Mutated IGHV (<98% homology):** Indolent disease; historical long-term|
|     plateaus with FCR, but targeted therapy remains preferred.              |
+-----------------------------------------------------------------------------+

Frontline Therapeutic Strategies in CLL

+-----------------------------------------------------------------------------+
|                  FRONTLINE CLL REGIMEN COMPARISON                           |
|                                                                             |
|   [STRATEGY 1: CONTINUOUS 2nd-GEN BTK INHIBITORS]                           |
|   - **Zanubrutinib (Brukinsa):** 160 mg PO BID or 320 mg daily              |
|     * SEQUOIA trial (frontline) & ALPINE trial (R/R vs ibrutinib): Superior |
|       PFS, higher complete response, and significantly lower atrial         |
|       fibrillation / cardiac toxicity vs ibrutinib.                         |
|   - **Acalabrutinib (Calquence):** 100 mg PO BID (+/- Obinutuzumab)         |
|     * ELEVATE-TN trial: Outstanding 5-year PFS.                             |
|     * Drug Interaction: Avoid PPIs (reduces solubility); separate H2RA by 2h|
|                                                                             |
|   [STRATEGY 2: FIXED-DURATION BCL-2 INHIBITOR (CLL14 TRIAL)]                |
|   - **Venetoclax + Obinutuzumab (12 Months Total Duration):**               |
|     * Obinutuzumab: 1,000 mg IV on D1 (100 mg), D2 (900 mg), D8, D15 (C1),  |
|       then Day 1 of Cycles 2-6 (total 6 cycles).                            |
|     * Venetoclax: Initiated on Cycle 1 Day 22 with standard 5-WEEK RAMP-UP, |
|       continuing at 400 mg daily to complete 12 total 28-day cycles.        |
|     * High rate of undetectable Minimal Residual Disease (uMRD < 10^-4).    |
+-----------------------------------------------------------------------------+

Venetoclax 5-Week Ramp-Up Protocol & TLS Risk in CLL

+-----------------------------------------------------------------------------+
|                 VENETOCLAX 5-WEEK RAMP-UP SCHEDULE IN CLL                   |
|                                                                             |
|   - Week 1:  **20 mg PO daily**                                             |
|   - Week 2:  **50 mg PO daily**                                             |
|   - Week 3:  **100 mg PO daily**                                            |
|   - Week 4:  **200 mg PO daily**                                            |
|   - Week 5+: **400 mg PO daily** (Target Full Dose)                         |
|                                                                             |
|   [TLS RISK STRATIFICATION (Howard / Cairo-Bishop Criteria)]                |
|   - **Low Risk:** All LN < 5 cm AND Absolute Lymphocyte Count (ALC) < 25k   |
|     * Outpatient hydration (1.5-2 L/d) + Oral Allopurinol 300 mg daily.     |
|   - **Medium Risk:** Any LN 5 to < 10 cm OR ALC >= 25k                      |
|     * Outpatient or inpatient; pre-dose labs at 0, 6, 8, 24 hr for W1 & W2. |
|   - **High Risk:** Any LN >= 10 cm OR (Any LN >= 5 cm AND ALC >= 25k)       |
|     * MANDATORY HOSPITALIZATION for 20 mg and 50 mg dose escalations.       |
|     * IV Hydration (150-200 mL/hr) + Allopurinol (or Rasburicase if high UA)|
|     * Intensive lab monitoring at 0, 6, 8, 12, 24 hours post-dose.          |
+-----------------------------------------------------------------------------+

Non-Covalent BTK Inhibitor & Relapsed CLL Management

  • Covalent BTK Inhibitor Resistance: Mutations at the C481 residue (e.g., BTK C481S) prevent irreversible covalent binding of ibrutinib, acalabrutinib, and zanubrutinib.
  • Pirtobrutinib (Jaypirca; BRUIN Trial): Highly selective, non-covalent (reversible) BTK inhibitor that inhibits both wild-type and C481-mutated BTK with nanomolar potency. Dose: 200 mg PO daily with or without food. Indicated for relapsed/refractory CLL post-covalent BTKi and post-venetoclax.
  • Richter's Transformation: Histologic transformation of CLL to aggressive Diffuse Large B-Cell Lymphoma (DLBCL; ~5–10% lifetime incidence). Managed with chemoimmunotherapy (R-CHOP), polatuzumab-R-CHP, or clinical trials.

3. Myeloproliferative Neoplasms (MPNs): PV, ET, and Myelofibrosis

Classical BCR-ABL1-negative MPNs arise from clonal hematopoietic stem cell proliferation driven by mutually exclusive somatic mutations in JAK2 (V617F exon 14 or exon 12), CALR (calreticulin exon 9 indels), or MPL (thrombopoietin receptor W515L/K).

+-----------------------------------------------------------------------------+
|                   MPN DRIVER GENETICS & DIAGNOSTIC PROFILES                 |
|                                                                             |
|   [POLYCYTHEMIA VERA (PV)]                                                  |
|   - Genetics: **JAK2 V617F (>95%)** or **JAK2 Exon 12 (3-4%)**              |
|   - Hallmark: Uncontrolled erythrocytosis, suppressed EPO, panmyelosis      |
|                                                                             |
|   [ESSENTIAL THROMBOCYTHEMIA (ET)]                                          |
|   - Genetics: **JAK2 V617F (55-60%)**, **CALR (25-30%)**, **MPL (3-5%)**    |
|   - Hallmark: Sustained thrombocytosis (platelets >= 450k), megakaryocytes  |
|                                                                             |
|   [PRIMARY MYELOFIBROSIS (PMF)]                                             |
|   - Genetics: **JAK2 V617F (55-60%)**, **CALR (25-30%)**, **MPL (5-8%)**    |
|   - Hallmark: Bone marrow reticulin/collagen fibrosis, leukoerythroblasto-  |
|     sis, teardrop poikilocytes, massive splenomegaly, constitutional symptoms|
+-----------------------------------------------------------------------------+

Polycythemia Vera (PV) Management Protocols

  • Cardiovascular Thrombosis Risk Stratification:
    • Low-Risk PV: Age < 60 years AND No history of thrombosis.
    • High-Risk PV: Age >= 60 years OR Prior arterial/venous thrombosis.
  • Therapeutic Core:
    1. Low-Dose Aspirin (81–100 mg daily): Reduces risk of thrombosis and cardiovascular death without excess bleeding (ECLAP trial).
    2. Therapeutic Phlebotomy: Mandatory in all patients to maintain Hematocrit STRICTLY < 45% (CYTO-PV trial: 4-fold reduction in cardiovascular death and major thrombosis vs target 45–50%).
    3. Cytoreductive Therapy (Mandatory in High Risk):
      • Hydroxyurea (500–1,500 mg daily): First-line oral ribonucleotide reductase inhibitor.
      • Ropeginterferon alfa-2b-njft (Besremi; PROUD-PV / CONTINUATION-PV): Monopegylated interferon administered SC every 2 to 4 weeks; induces deep molecular responses in JAK2 V617F allele burden.
      • Ruxolitinib (Jakafi; RESPONSE Trial): Indicated for PV resistant to or intolerant of hydroxyurea. Dose: 10 mg PO BID (titrated to 25 mg BID). Controls hematocrit without phlebotomy, reduces splenomegaly, and resolves pruritus.

Myelofibrosis (MF): Tailored JAK Inhibitor Therapeutics

+-----------------------------------------------------------------------------+
|                   MYELOFIBROSIS JAK INHIBITOR SELECTION MATRIX              |
+-----------------------------------------------------------------------------+
| 1. RUXOLITINIB (Jakafi) - Dual JAK1 / JAK2 Inhibitor (COMFORT-I/II Trials)   |
|    - Indication: Intermediate-2 or High-Risk MF; reduces spleen & symptoms  |
|    - Platelet-Guided Dosing:                                                |
|      * Platelets > 200,000 / mcL: **20 mg PO BID**                          |
|      * Platelets 100,000 - 200,000 / mcL: **15 mg PO BID**                  |
|      * Platelets 50,000 - <100,000 / mcL: **5 mg PO BID**                   |
|    - Pharmacist Mandate: **DO NOT STOP ABRUPTLY** (causes acute cytokine    |
|      rebound storm with severe shock and rapid spleen enlargement; taper!). |
|    - Monitor: Dose-dependent anemia/thrombocytopenia, zoster reactivation,  |
|      non-melanoma skin cancer, lipid elevations.                            |
|-----------------------------------------------------------------------------|
| 2. FEDRATINIB (Inrebic) - Selective JAK2 / FLT3 Inhibitor (JAKARTA Trials)  |
|    - Indication: Primary or secondary MF (frontline or post-ruxolitinib)    |
|    - Dose: 400 mg PO daily with high-fat meal (reduces GI toxicity)         |
|    - BLACK BOX WARNING: **Wernicke Encephalopathy (WE)**                    |
|      * PHARMACY MANDATE: Assess baseline **Thiamine (Vitamin B1) levels**   |
|        and monitor periodically. Do NOT start if thiamine is deficient!     |
|        Replete thiamine immediately if neurologic symptoms occur.           |
|-----------------------------------------------------------------------------|
| 3. PACRITINIB (Vonjo) - JAK2 / IRAK1 / ACVR1 Inhibitor (PERSIST-2 Trial)     |
|    - Indication: MF in patients with **SEVERE THROMBOCYTOPENIA (PLT < 50k)**|
|    - Dose: **200 mg PO BID** with food                                      |
|    - Unique Feature: Does NOT cause significant myelosuppression; inhibits  |
|      IRAK1 to downregulate inflammatory NF-kappaB signaling.                |
|-----------------------------------------------------------------------------|
| 4. MOMELOTINIB (Ojjaara) - JAK1 / JAK2 & ACVR1 / ALK2 Inhibitor (MOMENTUM)  |
|    - Indication: Intermediate or High-Risk MF with **ANEMIA**               |
|    - Dose: **200 mg PO daily** with or without food                         |
|    - Unique Mechanism: Blocks **Activin A Receptor Type 1 (ACVR1)**,        |
|      reducing hepatic **hepcidin** production, restoring iron availability, |
|      and stimulating erythropoiesis (improves transfusion independence!).   |
+-----------------------------------------------------------------------------+

Master Chronic Leukemia & MPN Comparative Matrix

MalignancyPrimary DriverHallmark RegimensKey Toxicities & Boxed WarningsEssential Pharmacist Action Points
CML (Chronic Phase)t(9;22) BCR::ABL1Dasatinib, Nilotinib, Imatinib, BosutinibPleural effusion (Dasatinib), QTc/AOE (Nilotinib), Diarrhea (Bosutinib)Avoid PPIs with Dasatinib; Nilotinib strictly on empty stomach; monitor qPCR on IS at 3, 6, 12 mo.
CML (T315I Mutation)BCR::ABL1 T315IPonatinib (45->15 mg) or Asciminib (200 mg BID)Arterial occlusive events, Pancreatitis, Heart failureDe-escalate Ponatinib dose upon response; Asciminib on empty stomach; vascular risk screening.
CLL (Frontline)del(17p), TP53, IGHV unmutatedZanubrutinib OR Venetoclax + ObinutuzumabAtrial fibrillation, Bleeding (BTKi), Severe TLS, Cytopenias (Venetoclax)5-week Venetoclax ramp-up with hydration/allopurinol; hold BTKi 3–7 days before invasive surgery.
CLL (R/R post-cBTKi)BTK C481S mutationPirtobrutinib (200 mg daily)Fatigue, Bruising, Neutropenia, rare AFibReversible non-covalent BTKi; effective despite C481S covalent-binding resistance.
Polycythemia VeraJAK2 V617F / Exon 12Phlebotomy + Aspirin +/- Hydroxyurea / RuxolitinibThrombosis, Pruritus, Myelosuppression, Skin cancerEnforce Hematocrit < 45% target strictly; baseline skin exams for Ruxolitinib.
Myelofibrosis (PLT <50k)JAK2, CALR, MPLPacritinib (200 mg BID)Diarrhea, Nausea, QTc prolongationSafe in severe thrombocytopenia; avoid concurrent strong CYP3A4 inhibitors/inducers.
Myelofibrosis (Anemic)JAK2, CALR, MPLMomelotinib (200 mg daily)Thrombocytopenia, Hepatotoxicity, NeuropathyBlocks ACVR1 to suppress hepcidin; improves hemoglobin and transfusion independence.
Test Your Knowledge

A 58-year-old male with chronic phase CML has been receiving dasatinib 100 mg PO daily for the past 6 months. His recent quantitative RT-PCR demonstrates a BCR::ABL1 transcript level of 8.2% on the International Scale (IS). During a comprehensive medication therapy management review, the oncology pharmacist discovers that 2 months ago, the patient was diagnosed with severe gastroesophageal reflux disease (GERD) by his primary care physician and was prescribed omeprazole 40 mg PO daily. How should the clinical oncology pharmacist assess and resolve this drug interaction?

A
B
C
D
Test Your Knowledge

A 64-year-old woman with relapsed CLL harboring a del(17p) and TP53 mutation progresses on frontline ibrutinib therapy. Molecular sequencing reveals a BTK C481S point mutation. The clinical team intends to initiate a non-covalent, reversible BTK inhibitor. Which of the following agents is FDA-approved for this specific clinical scenario, and what is its standard dosing regimen based on the BRUIN trial?

A
B
C
D
Test Your Knowledge

A 71-year-old male with intermediate-2 risk Primary Myelofibrosis presents with progressive fatigue, early satiety, massive splenomegaly (palpable 14 cm below the left costal margin), and profound cytopenias. Laboratory evaluation reveals: WBC 4.1 x 10^3/mcL, Hemoglobin 8.2 g/dL, and Platelet count 32 x 10^3/mcL (severe thrombocytopenia). The treating hematologist wishes to initiate a JAK inhibitor to control constitutional symptoms and splenomegaly. Which of the following JAK inhibitors is specifically indicated and FDA-approved for myelofibrosis in patients with baseline severe thrombocytopenia (platelet count < 50 x 10^3/mcL)?

A
B
C
D
Test Your Knowledge

A 66-year-old male with symptomatic, high-risk Primary Myelofibrosis is being started on fedratinib 400 mg PO daily following loss of response to ruxolitinib. Which of the following boxed warnings and mandatory pharmacist-led laboratory monitoring protocols is unique to fedratinib therapy?

A
B
C
D
Up Next

11.3 Multiple Myeloma & Plasma Cell Dyscrasias

Continue learning