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On December 4, 2020 Magenta Therapeutics (NASDAQ: MGTA) and bluebird bio, Inc. (NASDAQ: BLUE) reported an exclusive clinical trial collaboration to evaluate the utility of MGTA-145, in combination with plerixafor, for mobilization and collection of stem cells in adults and adolescents with sickle cell disease (SCD) (Press release, Magenta Therapeutics, DEC 4, 2020, View Source [SID1234639033]). The data from this clinical trial could provide proof-of-concept for MGTA-145, in combination with plerixafor, as the preferred mobilization regimen for patients with SCD. bluebird bio’s experience with plerixafor as a mobilization agent in sickle cell disease aligns with Magenta’s combination therapy approach, utilizing MGTA-145 plus plerixafor with potential to achieve safe, rapid and reliable mobilization of sufficient quantities of high-quality stem cells to improve outcomes associated with stem cell transplantation. Under the collaboration, the stem cells will be fully characterized, and Magenta will undertake preclinical studies to evaluate the ability of these cells to be gene corrected and engrafted in mouse models. The companies will co-fund the clinical trial and Magenta will retain all rights to its product candidate.

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This press release features multimedia. View the full release here: View Source

"We are excited to build upon our leading position in the field of ex-vivo gene therapy and the promising clinical data with LentiGlobin in SCD with a collaboration focused on achieving improved stem cell mobilization," said Dave Davidson, M.D., chief medical officer, bluebird bio. "In this initial study, we hope to establish whether the combination of plerixafor with MGTA-145 can generate appropriate CD34+ stem cells with a single round of mobilization. If successful, we hope to evaluate this novel mobilization regimen with LentiGlobin to make another step forward in the treatment of patients with SCD."

"Achieving reliable and rapid stem cell mobilization and a simplified collection process can ensure the entire patient experience is optimal with respect to therapeutic outcome. The incorporation of bluebird bio’s experience in this area of treatment will be immensely valuable in further developing MGTA-145 plus plerixafor to address the remaining unmet needs in gene therapy approaches for diseases like sickle cell disease," said John Davis Jr., M.D., M.P.H., M.S., Head of Research & Development and Chief Medical Officer, Magenta Therapeutics. "We look forward to collaborating with bluebird bio to evaluate MGTA-145 as the preferred mobilization option for people with sickle cell disease."

SCD is a serious, progressive and debilitating genetic disease caused by a mutation in the β-globin gene that leads to the production of abnormal sickle hemoglobin (HbS), causing red blood cells (RBCs) to become sickled and fragile, resulting in chronic hemolytic anemia, vasculopathy and painful vaso-occlusive events (VOEs). For adults and children living with SCD, this means unpredictable episodes of excruciating pain due to vaso-occlusion as well as other acute complications—such as acute chest syndrome (ACS), stroke, and infections, which can contribute to early mortality in these patients.

Currently available mobilization drugs, including granulocyte-colony stimulating factor (G-CSF), a commonly used mobilization agent administered over the course of five to seven days in other transplant settings, is not used in sickle cell disease because it can trigger vaso-occlusive crises and even death in adults and adolescents. Plerixafor is used to mobilize a patient’s stem cells for collection prior to transplant and while an available treatment option, multiple cycles of apheresis and collection may sometimes be required to generate sufficient stem cells for gene therapy. Magenta is developing MGTA-145, in combination with plerixafor, to be the preferred mobilization regimen for rapid and reliable mobilization and collection of hematopoietic stem cells (HSCs) to improve stem cell transplantation outcomes in multiple disease areas, including genetic diseases such as sickle cell disease, as well as blood cancers and autoimmune diseases.

About Magenta Therapeutic’s MGTA-145

MGTA-145, in combination with plerixafor, has demonstrated, in a recently completed Phase 1 study in healthy volunteers, it can rapidly and reliably mobilize high numbers of functional stem cells in a single day, without the need for G-CSF. MGTA-145 works in combination with plerixafor to harness a physiological mechanism of stem cell mobilization to rapidly and reliably mobilize HSCs for collection and transplant across multiple indications.

Additionally, as shown in preclinical studies, stem cells mobilized with MGTA-145 can be efficiently gene-modified and are able to engraft, potentially allowing for safer and more efficient mobilization for gene therapy approaches to treat sickle cell disease and other genetic diseases.

Magenta completed its Phase 1 trial of MGTA-145 in healthy volunteers, demonstrating MGTA-145 was well tolerated and enables same-day dosing, mobilization and simplified collection of sufficient stem cells for transplant, meeting all primary and secondary endpoints.

On December 4, 2020, Atara Biotherapeutics, Inc. (the "Company" or "Atara") reported that it entered into a Research, Development and License Agreement (the "License Agreement") with Bayer AG ("Bayer") (Filing, 8-K, Atara Biotherapeutics, DEC 4, 2020, View Source [SID1234572309]). Pursuant to the License Agreement, the Company grants to Bayer an exclusive, field-limited license under the applicable patents and know-how owned or controlled by the Company and its affiliates covering or related to ATA2271 and ATA3271, the Company’s next-generation CAR T immunotherapy programs targeting mesothelin, of which the Company is currently developing ATA2271 in collaboration with Memorial Sloan Kettering Cancer Center ("MSK"), to develop, manufacture and commercialize products comprising ATA2271 and ATA3271 and certain derivatives thereof ("Licensed Products"), in each case targeting mesothelin.

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Under the terms of the License Agreement, the Company will be responsible at its cost for all mutually agreed pre-clinical and clinical activities for ATA2271 through the first in human Phase 1 clinical study, following which Bayer will be responsible for the further development of ATA2271 at its cost. Bayer will be responsible for the development of ATA3271, except for certain mutually agreed pre-clinical, translational, manufacturing and supply chain activities to be performed by the Company relating to ATA3271, in each case at Bayer’s cost. Bayer will also be solely responsible for commercializing the Licensed Products at its cost. The Company will own any intellectual property rights developed solely by the Company under the collaboration, and Bayer will own any intellectual property rights developed solely by Bayer or jointly by the parties under the collaboration. Such Bayer-developed or jointly-developed intellectual property rights are subject to the Company’s rights to certain manufacturing and process development-related intellectual property. The Company has agreed to not develop or commercialize (or assist any third party to develop or commercialize) any cell therapy targeting mesothelin outside of the collaboration with Bayer for a period of three years from the first commercial sale of a Licensed Product.

Bayer will pay the Company an upfront cash payment of $45.0 million for the exclusive license grant, and will make an additional $15.0 million reimbursement payment to the Company for certain research and process development activities to be performed by the Company under the License Agreement. The Company is also entitled to receive (i) up to an additional $5.0 million for additional, specified pre-clinical and translational activities under the License Agreement, (ii) an aggregate of up to $610.0 million in milestone payments upon achieving certain development, regulatory and commercial milestones relating to Licensed Products and (iii) additional amounts for manufacturing services and product supply. In addition, the Company is eligible to receive tiered royalties at percentages up to low double digits on worldwide net product sales of Licensed Products on a country-by-country and product-by-product basis until the later of 12 years after the first commercial sale in such country or the expiration of specified patent rights in such country, subject to certain reductions and aggregate minimum floors. The License Agreement includes (i) various representations, warranties, covenants, indemnities, and other customary provisions and (ii) contains customary provisions for termination by Bayer for convenience, by the Company upon a challenge of the Company’s licensed patents, and by either party, including in the event of breach of the License Agreement (subject to cure), subject, in each case, to certain reversion rights, or upon the other party’s bankruptcy.

Pursuant to the License Agreement, for a limited period of time and only if the Company pursues a potential out-license of an additional Atara CAR T product candidate, the Company also grants Bayer a non-exclusive right to negotiate a license of such additional Atara CAR T product candidate on mutually agreed terms. The foregoing right granted to Bayer will expire upon certain change of control events of the Company.

The foregoing summary is qualified in its entirety by reference to the License Agreement. The License Agreement will be filed as an exhibit to the Company’s Annual Report on Form 10-K for the year ended December 31, 2020.

On December 4, 2020 AB Science SA (Euronext-FR0010557264-AB) reported that its Phase 3 study (AB12005-NCT03766295) met its primary objective to demonstrate increase in survival in pancreatic cancer with pain (Press release, AB Science, DEC 4, 2020, View Source [SID1234572271]).

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Study AB12005 evaluated masitinib 6.0 mg/kg/day in combination with gemcitabine in first-line treatment of unresectable locally advanced or metastatic pancreatic cancer patients with pain. The study was successful if its primary objective to test a significant increase in overall survival was reached at a 2.5% level of statistical significance in either the overall population with pain or in the population with unresectable locally advanced tumors with pain.

In the population with unresectable locally advanced tumors with pain, the masitinib treatment-arm showed a significant improvement in overall survival (OS) relative to the control arm. The between group difference in median OS was 1.8 months (p=0.007) in favor of masitinib (13.0 months in masitinib arm versus 11.2 months in control group), with a 0.46 hazard ratio (HR) of death, which represents a reduction in risk of death of 54% for masitinib-treated patients relative to control. Results on the primary endpoint were consistent with secondary analysis in progression free survival (PFS), which measures the time to tumor progression or death (whichever occurs first) from the start of treatment. The between group difference in median PFS was 1.8 months (p=0.039) in favor of masitinib (7.4 months in masitinib arm versus 5.6 months in control group), with a 0.47 hazard ratio representing a reduction in risk of having a progression or death of 53%.

Masitinib also reduced pain relative to the control arm in patients with unresectable locally advanced tumors, as demonstrated by a between group difference that reached statistical significance or approached significance at each timepoint. In pancreatic cancer, there is evidence that pain is a clinical predictor of poor prognosis [1]. Study AB12005 demonstrated that mast cells are associated with pain and that blocking mast cells, as masitinib does, is able to reverse the poor prognosis of patients with unresectable locally advanced tumors with pain.

In the overall population including both locally advanced and metastatic pancreatic cancer patients with pain, no survival benefit was detected, suggesting that masitinib treatment should be initiated early in the course of the disease, prior to metastasis.

From the first Phase 3 study AB07012 [2] and literature [3], around 50% of patients with pancreatic cancer had pain intensity (VAS > 20) and 25% to 50% of pancreatic cancer patients are patients with unresectable locally advanced tumors.

The safety of masitinib 6.0 mg/kg/day in combination with gemcitabine compared favorably to that of gemcitabine as a single agent, with fewer adverse event and severe adverse events reported in the masitinib arm as compared with the control arm:
-96.3% of patients had at least one adverse event in masitinib arm versus 99.3% in the control arm
-18.7% of patients had one fatal adverse event in masitinib arm versus 19.1% in the control arm
-19.1% of patients had at least one serious adverse event (non-fatal) in masitinib arm versus 21.3% in the control arm
-74.8% of patients had at least one adverse event with Grade 3 or 4 in masitinib arm versus 83.1% in the control arm Page 2/5 Study AB12005 was a confirmatory Phase 3 study.

The first Phase 3 study (AB07012) was a hypothesis generating study and identified that patients with pain had a median OS increased by 2.6 months (p=0.012) with masitinib as compared to control. Study AB12005 demonstrated that there is a benefit generated by masitinib for pancreatic cancer patients with pain, provided that treatment is initiated prior to metastasis.

Dr. Joël Ezenfis, MD, principal coordinating investigator of the study, said: "We are very pleased that this study is successful. The increase of 1.8 months in median overall survival for masitinib-treated patients is clinically relevant as this population of patients suffers from a condition with very limited treatment options and survival rate has remained stubbornly poor despite decades of clinical studies."

Julien Taieb, MD, PhD, Head of the Gastroenterology and Gastrointestinal Oncology Department at the Georges Pompidou European Hospital said: "Masitinib is not a cytotoxic agent but a targeted drug blocking two cells of the innate immune system, mast cells and macrophages. Study AB12005 demonstrated for the first time that this targeted approach is beneficial in a targeted population, made of patients with unresectable locally advanced tumors with pain".

Prof. Olivier Hermine, president of the Scientific Committee of AB Science and member of the Académie des Sciences in France, said: "This study is particularly important as it confirms the relevance of targeting mast cells and macrophages in oncology. We had previously observed the benefit of masitinib targeting mast cells and macrophages in cancer through in vitro and in animal assays in my laboratory. This study validates the benefit of masitinib in humans in the most difficult-to-treat cancer. We can now state that masitinib is an anti-metastatic drug that could be useful in patients at high risk of developing metastases. In addition, it validates the role of mast cells in pain and the acceptable safety profile of masitinib even in combination with chemotherapy."

Alain Moussy, co-founder and CEO of AB Science said: "This is a major achievement for masitinib in oncology. The next step is to discuss with the Health Authorities a potential filing for marketing authorization application of masitinib in the first line treatment of unresectable locally advanced pancreatic cancer associated with pain". AB Science plans to present complete study results at an upcoming medical meeting.

AB12005 Study Design Study AB12005 was a randomized, placebo-controlled, phase 3 study of masitinib in first-line treatment of unresectable locally advanced or metastatic pancreatic cancer patients with pain at baseline or taking opioids. The pre-specified primary endpoint was overall survival.

The primary analysis was pre-specified both in the overall population and also in patients with unresectable locally advanced tumors, with a 5% alpha spending split, which corresponds to the chance factor threshold below which the statistical test is considered significant by regulatory authorities, of 2.5% for the overall population and 2.5% for the locally advanced subgroup.

The distinction between unresectable locally advanced or metastatic disease status was a stratification factor, thereby ensuring that treatment-arms were unbiased for this known prognostic factor. Secondary endpoints included progression free survival according to central RECIST criteria and change in pain from baseline. The study enrolled 383 patients (randomization 2:1 between masitinib and placebo) with i) histologically or cytologically confirmed adenocarcinoma of the pancreas, unresectable locally advanced or metastatic stage, ii) pain related to the disease (Visual Analogue Scale > 20 mm or opioid analgesics at a dose ≥ 1 mg/kg/day), and iii) chemotherapy naïve for the advanced/metastatic disease. 92 patients had unresectable locally advanced with pain criteria. Page 3/5 Efficacy analysis was performed in the modified intent-to-treat (mITT) population, which included all randomized patients who took at least one dose of study treatment (masitinib/placebo) and with pain criteria (VAS > 20 and/or patients treated with opioid analgesics dose ≥ 1 mg/kg/day at baseline).

There was a difference of 4 patients between the ITT population and the mITT population, with 1 patient receiving no study treatment and 3 patients without pain criteria. Rationale for developing masitinib in patients with pancreatic cancer with pain A first phase 2/3 study (AB07012) enabled the identification of a subgroup based on the level of pain at baseline where survival was statistically increased (+2.6 months, p=0.012, Hazard Ratio=0.62). Pain intensity was assessed via a visual analog scale (VAS) at baseline. This linear scale provides a visual representation of pain as perceived by the patient. Pain intensity was represented by a 100 mm long, continuous line free of any internal reference marks. One extremity indicated an absence of pain (0-value) and the other extremity indicated very severe pain (100-value).

The VAS threshold for the ‘pain’ subgroup was set to VAS ≥20 mm, which is consistent with established precedent from the scientific literature [3-6]. There is evidence from the scientific literature in support of biological plausibility for the observed masitinib treatment-effect in patients with baseline pain (VAS ≥ 20). The presence of pain in pancreatic cancer is thought to flag an increased mast cell activity within the tumor microenvironment, which promotes disease progression. Masitinib’s highly selective inhibition of mast cell activation is expected to be of therapeutic benefit by modulating mast cell related remodeling of the tumor microenvironment.

About pancreatic cancer
The estimated prevalence of people living with pancreatic cancer is 21 per 100,000 [7]. At the time of diagnosis, most patients with pancreatic ductal adenocarcinoma present with locally advanced or metastatic disease and only 10-20% of cases are candidates for curative surgery. Median overall survival is between 6 to 7 months and 1-year survival rates range between 17 to 25% [8;9]. As such, population with unresectable pancreatic cancer in first line is around 100,000 in the EU and 60,000 in the USA. From the first Phase 3 study AB07012 [2] and literature [3], around 50% of patients with pancreatic cancer had pain intensity (VAS > 20) and 25% to 50% of pancreatic cancer patients are patients with unresectable locally advanced tumors

Reference
[1] Okusaka T, et al. Abdominal pain in patients with resectable pancreatic cancer with reference to clinicopathologic findings. Pancreas. 2001;22(3):279-284.
[2] Deplanque 2015, Ann Oncol. doi: 10.1093/annonc/mdv133. View Source
[3] Balaban EP, et al. Locally Advanced Unresectable Pancreatic Cancer: American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Clinical Practice Guideline Summary. J Oncol Pract. 2017 Apr;13(4):265-269. doi: 10.1200/JOP.2016.017376. [3] Khazaie K, Blatner NR, Khan MW, et al. The significant role of mast cells in cancer. Cancer Metastasis Rev. Mar 2011;30(1):45-60. [4] Theoharides TC. Mast cells and pancreatic cancer. N Engl J Med. Apr 24 2008;358(17):1860-1861.
[5] Maltby S, Khazaie K, McNagny KM. Mast cells in tumor growth: angiogenesis, tissue remodelling and immunemodulation. Biochim Biophys Acta. Aug 2009;1796(1):19-26.
[6] Christy AL, Brown MA. The multitasking mast cell: positive and negative roles in the progression of autoimmunity. J Immunol. Sep 1 2007;179(5):2673-2679
[7] National Cancer Institute, Pancreatic Cancer statistics, 2015
[8] Heinemann V, et al. BMC Cancer. 2008;8:82.
[9] Von Hoff DD, et al. N Engl J Med. Oct 31 2013;369(18):1691-1703. Page 4/5

About masitinib
Masitinib is a new orally administered tyrosine kinase inhibitor that targets mast cells and macrophages, important cells for immunity, through inhibiting a limited number of kinases. Based on its unique mechanism of action, masitinib can be developed in a large number of conditions in oncology, in inflammatory diseases, and in certain diseases of the central nervous system. In oncology due to its immunotherapy effect, masitinib can have an effect on survival, alone or in combination with chemotherapy. Through its activity on mast cells and microglia and consequently the inhibition of the activation of the inflammatory process, masitinib can have an effect on the symptoms associated with some inflammatory and central nervous system diseases and the degeneration of these diseases.

On December 4, 2020 Johnson & Johnson reported that New data from the Phase 2 CAPTIVATE study (PCYC-1142) were presented today during an oral session at the 2020 American Society of Hematology (ASH) (Free ASH Whitepaper) Annual Meeting (Abstract #123) (Press release, Johnson & Johnson, DEC 4, 2020, View Source;Based-Regimen-as-Fixed-Duration-First-Line-Treatment-for-Patients-with-Chronic-Lymphocytic-Leukaemia [SID1234572247]).1 The study evaluated the efficacy and safety of IMBRUVICA (ibrutinib) plus venetoclax in the treatment of adult patients with chronic lymphocytic leukaemia (CLL) and showed that, after achieving undetectable minimal residual disease (uMRD) in both the blood and bone marrow with the ibrutinib combination regimen, the one-year disease-free survival (DFS) of patients randomised to discontinue active treatment was comparable to that of patients randomised to continue ibrutinib monotherapy (95.3 percent vs. 100 percent, respectively [p=0.1475]).1

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"These data demonstrate the potential of this oral, once-daily, chemotherapy-free combination regimen in first-line treatment of CLL," said William Wierda,* M.D., Professor, Department of Leukemia, The University of Texas MD Anderson Cancer Center and principal study investigator. "Once-daily treatment with ibrutinib remains the established standard of care in CLL; the latest results from the CAPTIVATE study underscore that the mechanistic synergy of ibrutinib and venetoclax delivers deep MRD remissions in the blood and bone marrow and enables treatment-free periods for patients."

The CAPTIVATE trial is evaluating adult patients younger than 70 years, including patients with high-risk disease, in two cohorts: an MRD Guided Cohort where treatment duration is guided by the patient’s MRD status after 12 cycles of combination ibrutinib plus venetoclax therapy; and a Fixed Duration Cohort where all patients stop therapy after 12 cycles of the combination, regardless of MRD status. Patients in the MRD Guided Cohort (n=164; median age, 58 years) who achieved uMRD, defined as having uMRD (<10–4 by 8-color flow cytometry) serially over at least three cycles and undetectable MRD in both peripheral blood (PB) and bone marrow (BM) with combination therapy, were randomised in a double-blinded fashion to continue treatment with ibrutinib monotherapy or placebo until disease progression.1

Patients in the MRD Guided Cohort who did not achieve uMRD following 12 cycles of combination ibrutinib plus venetoclax therapy were randomised to continue ibrutinib monotherapy or the combination.1 With a median total treatment duration of 28.6 months (range, 0.5-39.8) with ibrutinib and 12.0 months (range, 0.8-34.1) with venetoclax, increases in uMRD rates were greater with continued combination therapy versus continued ibrutinib monotherapy.1,2 Across all four randomised arms, 30-month progression-free survival rates were 95 percent or greater.1,2

The safety profile of the ibrutinib plus venetoclax regimen was consistent with known safety profiles of the individual therapies.1 Across all treated patients, the most common grade 3/4 adverse events (AEs) were neutropenia (36 percent), hypertension (10 percent), thrombocytopenia (5 percent), and diarrhoea (5 percent).1

"Ibrutinib is the only Bruton’s tyrosine kinase inhibitor that has shown significant overall survival and progression-free survival benefits in randomised Phase 3 studies in first-line CLL, and it continues to demonstrate efficacy and safety across regimens and patient subgroups, including those with historically poor outcomes," said Craig Tendler, M.D., Vice President, Late Development and Global Medical Affairs, Oncology, Janssen Research & Development, LLC. "Results from the randomised phase of the MRD Guided Cohort of the CAPTIVATE study show that treatment-free remissions are possible with ibrutinib-based fixed duration therapy, providing yet another treatment option for patients starting first-line CLL treatment."

"Ibrutinib has impacted more than 200,000 patients worldwide and the CAPTIVATE study provides more evidence in support of the lasting effect that can be achieved in people living with CLL over time," adds Dr Catherine Taylor, Vice President, Medical Affairs Therapeutic Area Strategy, Europe, Middle East and Africa (EMEA), Janssen-Cilag Ltd., Middle East. "The manageable safety profile of the ibrutinib combination with a low rate of discontinuation underscores this regimen as a potential viable option and we are excited to explore how it can benefit patients in a front-line setting."

The registrational Phase 3 GLOW study, assessing ibrutinib plus venetoclax in comparison to chlorambucil plus obinutuzumab for first-line treatment of elderly or younger unfit patients with CLL (NCT03462719) is ongoing as part of the comprehensive development programme exploring the potential of ibrutinib-based fixed duration therapy.3

*William Wierda is the lead investigator of the CAPTIVATE study. He was not compensated for any media work.

#ENDS#

About Ibrutinib
Ibrutinib is a once-daily, first-in-class Bruton’s tyrosine kinase (BTK) inhibitor that is administered orally, and is jointly developed and commercialised by Janssen Biotech, Inc. and Pharmacyclics LLC, an AbbVie company.4 Ibrutinib blocks the BTK protein; the BTK protein sends important signals that tell B cells to mature and produce antibodies. BTK signalling is needed by specific cancer cells to multiply and spread.5 By blocking BTK, ibrutinib may help move abnormal B cells out of their nourishing environments in the lymph nodes, bone marrow, and other organs.6

Indications for which ibrutinib is approved in Europe include:3

Chronic lymphocytic leukaemia (CLL): As a single agent or in combination with rituximab or obinutuzumab for the treatment of adult patients with previously untreated CLL, and as a single agent or in combination with bendamustine and rituximab (BR) for the treatment of adult patients with CLL who have received at least one prior therapy
Mantle cell lymphoma (MCL): As a single agent for the treatment of adult patients with relapsed or refractory MCL
Waldenström’s macroglobulinemia (WM): As a single agent for the treatment of adult patients who have received at least one prior therapy or in first-line treatment for patients unsuitable for chemo-immunotherapy, and in combination with rituximab for the treatment of adult patients
Ibrutinib is approved in more than 100 countries for at least one indication, and to date, has been used to treat more than 200,000 patients worldwide.7

For a full list of side effects and information on dosage and administration, contraindications and other precautions when using ibrutinib please refer to the Summary of Product Characteristics for further information.

About Chronic Lymphocytic Leukaemia
Chronic lymphocytic leukaemia (CLL) is typically a slow-growing blood cancer of the white blood cells.8 The overall incidence of CLL in Europe is approximately 4.92 cases per 100,000 persons per year and is about 1.5 times more common in men than in women.9 CLL is predominantly a disease of the elderly, with a median age of 72 years at diagnosis.10

The disease eventually progresses in the majority of patients, and they are faced with fewer treatment options with each relapse. Patients are often prescribed multiple lines of therapy as they relapse or become resistant to treatments.