Oncolytics Biotech® Inc. Collaborators Present REOLYSIN® Preclinical Data at the 9th International Conference on Oncolytic Virus Therapeutics

On June 15, 2015 Oncolytics Biotech reported that a series of oral and poster presentations are being made by the Company’s research collaborators at the 9th International Conference on Oncolytic Virus Therapeutics being held from June 13th to 16th, 2015 in Boston MA (Press release, Oncolytics Biotech, JUN 15, 2015, View Source [SID:1234505435]).

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"Our preclinical program continues to identify new potential therapeutic combinations as well as advance our understanding of how REOLYSIN works," said Dr. Brad Thompson, President and CEO of Oncolytics. "This work is an important part of the ongoing development of our proprietary formulation of the human reovirus."

Dr. Richard Vile is making an oral presentation regarding previously disclosed findings around augmenting tumor-specific natural killer (NK) responses and specifically attenuating tumor-specific immunosuppression. These data also suggest that the combination of PD-1 inhibition therapy with reovirus oncolytic/immunotherapy represents a readily translatable method to enhance the therapeutic efficacy.

The first abstract/poster titled "Targeting peripheral and lymph node resistant CLL with combination reovirus therapy," was authored by Melcher, et al. The authors studied chronic lymphocytic leukemia ("CLL") and the problems associated with eradicating minimal residual disease and drug resistance. They concluded that the combination of reovirus and ABT-263 could increase direct and immune-mediated killing of peripheral disease and that reovirus in combination with Fludarabine may be useful in targeting drug-resistant lymph node disease.

The second abstract/poster titled "Oncolysis by reovirus as an immune priming mechanism with VSV-cDNA immunological boosting treats large established tumors," was authored by Melcher, et al. The authors looked at the treatment of established B16 melanoma tumors in a mouse model. They concluded that the local killing of cancer cells by one virus primed the immune system and, by using tumor antigens expressed from a second virus, it was possible to generate potent immunological responses that led to the rejection of well established tumors.

The third abstract/poster titled "Monocyte carriage and delivery of reovirus-antibody complexes for melanoma oncolysis," was authored by Melcher, et al. The authors studied preexisting antiviral immunity and found evidence that there is an alternative mechanism by which systemically administered reovirus may gain access to tumors, even in the presence of neutralizing antibodies.

8-K – Current report

On June 15, 2015 Karyopharm Therapeutics reported the presentation of positive clinical data for its lead product candidate, selinexor (KPT-330), a first-in-class, oral Selective Inhibitor of Nuclear Export / SINE compound, at the 20th Congress of the European Hematology Association (EHA) (Free EHA Whitepaper) 2015 Annual Meeting held June 11-14, 2015 in Vienna, Austria (Filing, 8-K, Karyopharm, JUN 15, 2015, View Source [SID:1234505437]).

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In an ongoing Phase 1b company-sponsored clinical trial evaluating the activity of single-agent selinexor (doses of 3-80mg/m2) in heavily pre-treated patients with diffuse large B-cell lymphoma (DLBCL), selinexor demonstrated a 43% overall response rate (partial response or better) in patients on study greater than one month, and a 31% overall response rate across all doses in the intention to treat population, with a median duration of response (DOR) of greater than nine months. Similar responses were observed in both GCB and non-GCB subtypes. The median overall survival (OS) and progression free survival (PFS) were 4.6 months and 1.7 months, respectively, for the entire study. In patients with a response to selinexor (N=12), the median OS was greater than 10 months (median not reached) and PFS was 24 months, significantly longer than those without a response (N=27; OS 3.5 months, PFS 1.2 months). Adverse events were manageable with standard supportive care and clinically significant cumulative toxicities were not observed, with several patients remaining on selinexor for more than one year.

Additional clinical data on selinexor’s activity in DLBCL, including in patients with double-hit DLBCL, will be provided in an oral presentation on Saturday June 20, 2015, at 10:50 CEST by Dr. Ramiro Garzon from the Ohio State University at the 13th International Conference on Malignant Lymphoma (ICML) in Lugano, Switzerland.

Initial data from the ongoing Selinexor AraC Idarubicin Leukemia, or "SAIL," study, an investigator-sponsored Phase 2 clinical trial of selinexor with intensive chemotherapy (idarubicin and cytosine arabinoside [Ara-C]) in patients with acute myeloid leukemia (AML) that relapsed after standard intensive induction chemotherapy, were also reported. In 18 evaluable patients, the combination of selinexor (40 mg/m2) with idarubicin/Ara-C demonstrated a 56% overall response rate, including nine patients with complete remission (CR/CRi) and one patient with a partial remission. Adverse events were manageable with standard supportive care and dose adjustments.

"We are excited by these promising data presented at EHA (Free EHA Whitepaper), which continue to demonstrate the vast potential of selinexor across hematologic malignancies and provide further evidence of selinexor’s broad and durable activity, both as a single agent and in combination therapy," said Sharon Shacham, PhD, MBA, President and Chief Scientific Officer of Karyopharm. "The correlation between response and prolonged survival demonstrated in heavily pretreated DLBCL patients suggests that responses to selinexor may confer a clinical benefit in this very difficult to treat population and support the ongoing

SADAL study in this group of patients. Moreover, the preliminary clinical data in patients with relapsed/refractory AML suggest that selinexor can be combined effectively with manageable side effects. These findings represent the reported clinical data of selinexor in combination with intensive chemotherapy and suggest that selinexor can enhance the activity of these agents with manageable side effects."

Selinexor data in DLBCL were described during an oral presentation by Dr. Ramiro Garzon of the Ohio State University on Saturday, June 13, entitled "Patients with Heavily Pretreated Diffuse Large B-Cell Lymphoma (DLBCL) who Respond to Oral Selinexor Therapy Show Prolonged Survival: Updated Phase 1 Results." These data from an ongoing Phase 1b clinical study of single-agent selinexor (3-80 mg/m2 oral doses) in patients with DLBCL were as of June 1, 2015 and included the following highlights:

• Among 28 response evaluable patients (per protocol defined as those patients on study for at least one month), the ORR was 43% and the disease control rate (stable disease or better) was 71%. Responses included four patients (14%) who achieved a complete response as confirmed by PET scan, eight patients (29%) who achieved a partial response and 8 patients (29%) with stable disease.

• Among 39 patients treated across all doses, the ORR was 31% and the disease control rate (stable disease or better) was 51%.

• Duration of response was greater than nine months.

• Patients with a response to selinexor (N=12), achieved OS of greater than ten months (median not reached) and PFS of 24 months which were significantly longer than those without a response (N=27; OS 3.5 months, PFS 1.2 months).

• The median overall survival (OS) and progression free survival (PFS) were 4.6 months and 1.7 months, respectively, for the entire study.

• Selinexor showed similar activity in both GCB and non-GCB subtypes of DLBCL.
In a late-breaking poster presented on Saturday, June 13, entitled "Preliminary Phase II Results of Ara-C And Idarubicin in Combination with Selective Inhibitor of Nuclear Export (SINE) Compound Selinexor (KPT-330) in Patients with Relapsed or Refractory AML," Dr. Walter Fiedler of the University Medical Center Hamburg and colleagues described preliminary data from the ongoing Phase 2 SAIL clinical trial demonstrating that selinexor in combination with standard doses of Ara-C and idarubicin is a potentially effective strategy for treating patients with AML that was relapsed or refractory after at least one line of chemotherapy. All data are as of April 27, 2015 and highlights include:

• An overall response rate of 56% was achieved based on 18 evaluable patients with three patients (17%) achieving complete remission (CR), six patients (33%) achieving complete remission with incomplete blood count recovery (CRi) and one patient (6%) achieving partial remission (PR).

• Ten patients (56%) received or were expected to receive either stem cell transplant or donor lymphocyte infusion.

• Adverse events were manageable with standard supportive care and dose adjustments.
An additional poster was presented on Saturday, June 13, entitled "XPO1 Inhibition Using Selinexor Synergizes with Chemotherapy in Acute Myeloid Leukemia (AML) by Targeting DNA Repair Genes" by Dr. Romero Garzon of the Ohio State University. In that preclinical study, Dr. Garzon and colleagues showed that selinexor synergizes with anthracyclines and other topoisomerase 2 inhibitors by preventing AML cells from repairing their DNA after damage by the chemotherapy. This study provides the scientific rationale for the ongoing SAIL study described above and additional studies with topoisomerase 2 inhibitors, as well as mechanistic insights into the use of selinexor with other chemotherapeutic agents.

About Selinexor
Selinexor (KPT-330) is a first-in-class, oral Selective Inhibitor of Nuclear Export / SINE compound. Selinexor functions by binding with and inhibiting the nuclear export protein XPO1 (also called CRM1), leading to the accumulation of tumor suppressor proteins in the cell nucleus, which subsequently reinitiates and amplifies their tumor suppressor function. This is believed to lead to the selective induction of apoptosis in cancer cells, while largely sparing normal cells. Over 900 patients have been treated with selinexor in company- and investigator-sponsored Phase 1 and Phase 2 clinical trials in advanced hematologic malignancies and solid tumors. Karyopharm has initiated four registration-directed clinical trials of selinexor, including one in older patients with acute myeloid leukemia (SOPRA), one in patients with Richter’s transformation (SIRRT) and one in patients with diffuse large B-cell lymphoma (SADAL). A single-arm trial of selinexor in patients with multiple myeloma (STORM) that is also intended to be registration-directed was initiated in May 2015. In solid tumors, Karyopharm plans to initiate a registration-directed trial of selinexor to treat liposarcoma during the second half of 2015. Additional Phase 1 and Phase 2 studies are ongoing or currently planned, including multiple studies in combination with one or more approved therapies in a variety of tumor types to further inform the company’s clinical development priorities for selinexor. The latest clinical trial information for selinexor is available at www.clinicaltrials.gov.

Actavis plc is now Allergan plc

On June 15, 2015 Actavis reported that the company has adopted Allergan plc (NYSE: AGN) as its new global name and will begin trading today under a new symbol — AGN — after ringing The Opening Bell at the New York Stock Exchange (Press release, Actavis, JUN 15, 2015, View Source;p=RssLanding&cat=news&id=2059261 [SID:1234505439]). The company name change follows the acquisition of Allergan in March 2015 and the approval of the name change by Actavis shareholders on June 5. The combination of Allergan and Actavis created one of the world’s top 10 pharmaceutical companies by revenue and a leader in a new industry model – Growth Pharma.

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"Today is an exciting day for Allergan and our 30,000 employees around the world who have helped us reach this special moment," said Brent Saunders, CEO and President of Allergan. "By adopting the Allergan name, we are ensuring that our corporate identity reflects the transformation of our company within the pharmaceutical industry and our position as a dynamic new breed of company – a leader in Growth Pharma. Today, under one company name and identity, we set out on a new path forward, encouraging our employees across the globe to be bold in how we think and act, to engage and to move quickly to meet the needs of physicians, patients and customers.

"Allergan is home to world-renowned brands, the best-in-class global generics business, a premier pharmaceutical pipeline of medicines including brands, generics, biosimilars, OTC products and devices, as well as the fourth largest distributor in the U.S., which will retain the name Anda. Allergan’s fully integrated business provides unique opportunities to respond quickly to customer and patient needs, and change the lives of those who depend on us."

Allergan has initiated a rebranding campaign that will guide the transition of its facilities, operations and commercial presence around the world to the new company name. The company has launched a new global web site at www.Allergan.com. Based on feedback received from customers, the company’s U.S. and Canadian generics business will continue to operate under the Actavis name, capitalizing on its exceptional brand equity among customers.

Allergan has also today adopted a distinctive redesign of the company identity and logo. The new icon in the logo speaks to the strength of the Company’s unique capabilities, the energy and passion of its people and its forward momentum. The circular shapes personify movement; purposeful paths of change and growth; growing spheres of influence and ideas; and achievement across brands and generics.

The result is a new, momentum-building and accessible visualization that celebrates Allergan’s emergence as a Growth Pharma leader. Together, all united, all moving, resulting in an evolving, growing Company focused on a singular purpose – to power bold ideas in healthcare for people around the world.

Tosedostat In Combination With Low Dose Cytarabine Achieves Primary Endpoint In Phase 2 Study In Elderly Patients With AML

On June 15, 2015 CTI BioPharma reported findings from an investigator-sponsored Phase 2 trial in patients with either primary (de novo) acute myeloid leukemia (AML) or AML that has evolved from myelodysplastic syndrome (MDS) (Press release, CTI BioPharma, JUN 14, 2015, View Source;p=RssLanding&cat=news&id=2059047 [SID:1234505424]). Results showed the combination of tosedostat with low dose cytarabine/Ara-C (LDAC) resulted in an overall response rate (ORR) of 54 percent in elderly patients with AML – with 45 percent of patients achieving durable complete responses (CR). These final results were presented by Dr. Giuseppe Visani, Director of Hematology and Stem Cell Transplant Center at AORMN, Pesaro, Italy in a poster session (abstract #P564) during the 20th Congress of the European Hematology Association (EHA) (Free EHA Whitepaper), June 11-14, 2015 in Vienna, Austria.

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AML is the most common acute leukemia affecting adults, and its incidence increases with age. AML may develop from the progression of other diseases, such as MDS, which is a blood cancer that also affects the bone marrow and leads to a decrease in circulating red blood cells. Tosedostat is a potential first-in-class selective inhibitor of aminopeptidases, which are required by tumor cells to provide amino acids necessary for growth and tumor cell survival.

"Both the types and length of responses in this trial with tosedostat are very encouraging – particularly given the limited options and poor outcomes historically observed in elderly patients with acute myeloid leukemia, either de novo or secondary after myelodysplastic syndrome," said Dr. Visani. "Importantly, through this study we have also identified potential biomarkers that may help identify high-risk patients in which we are more likely to see these clinically meaningful results – the findings of which are quite compelling and warrant further study."

Findings Presented at EHA (Free EHA Whitepaper)
Final results presented at EHA (Free EHA Whitepaper) show that responding patients had a significant improvement in overall survival based on response rates compared to non-responding patients (p=0.018). In the intent-to-treat population (ITT), the ORR was 54 percent – with CR observed in 45 percent of patients (n=15/33). In the responding patients, the median time for achieving best response was 74 days (range: 22-145 days) and 55 percent (n=10/18) were still in remission after a median follow-up of 319 days. Safety analysis show that tosedostat in combination with LDAC was generally well tolerated. The primary adverse events observed were pneumonitis (12 percent), cardiac (6 percent), brain hemorrhage (3 percent), and asthenia (3 percent).

One of the secondary endpoints was to identify possible biomarkers associated with sensitivity and/or drug resistance. A gene expression profile (GEP) was performed on purified AML cells obtained from 29 patients. Analysis of these patient cells identified a molecular signature associated with clinical response (CR vs. no CR). Based on the differentially expressed genes (n=212), samples were divided according to either CR or no CR. Results showed that these differentially expressed genes were associated with relevant biological functions and pathways – including B-catenin (beta-catenin), TNFA-NFkB, ERB2, inflammatory response, and epithelial-mesenchimal transition – and showed that the achievement of a CR could be efficiently predicted by GEP.

"The results observed with tosedostat in acute myeloid leukemia add to a growing body of data showing the anti-tumor activity of this aminopeptidase inhibitor and the potential of using this approach to treat blood-related cancers," Alan K. Burnett, M.D., Global Lead for Myeloid Diseases at CTI BioPharma. "Based on the clinical data observed to date, we are advancing the development for tosedostat including the potential for a Phase 3 registrational study for primary acute myeloid leukemia or acute myeloid leukemia that evolves from myelodysplastic syndrome."

About the Study Design
The Phase 2 multicenter clinical trial was designed to assess tosedostat (orally once-daily) in combination with intermittent LDAC (twice daily) in 33 elderly patients (median age = 75 years) with either primary AML or secondary AML after MDS. Courses of LDAC were repeated every four weeks for up to eight cycles in the absence of disease progression or unacceptable toxicity. The primary objective was to exceed the upper limit of institutional expected CR rates (P0=10%, P1= 25%, α=0.05, 1-β=80%); secondary objectives include safety and toxicity, stable disease, overall survival, and progression-free survival as well as the identification of a possible biomarker associated with sensitivity and/or disease resistance through global gene expression profiling (GEP, Affymetrix Transciptome Array 2.0).

The poster for Abstract #P564 – "Tosedostat plus low dose cytarabine induces a high rate of responses that can be predicted by genetic profiling in AML: Final results of a Phase II multicenter study" – is available at www.ctibiopharma.com.

About Tosedostat
Tosedostat is an oral aminopeptidase inhibitor that has demonstrated anti-tumor responses in blood-related cancers and solid tumors in Phase 1-2 clinical trials. Tosedostat is currently being evaluated in multiple Phase 2 clinical trials for the treatment of patients with AML or high-risk MDS and are intended to inform the design of a Phase 3 registration study to support potential regulatory approval. Tosedostat is not approved or commercially available.

About Acute Myeloid Leukemia and Myelodysplastic Syndrome
AML is a cancer characterized by the rapid growth of abnormal white blood cells that accumulate in the bone marrow and interfere with the production of normal blood cells. AML is the most common acute leukemia affecting adults, and its incidence increases with age.1 The symptoms of AML are caused by the replacement of normal bone marrow with leukemic cells, which causes a drop in red blood cells, platelets, and normal white blood cells, leading to infections and bleeding. AML progresses rapidly and is typically fatal within weeks or months if left untreated. In 2015, approximately 20,830 new cases of AML are expected to be diagnosed in the United States and an estimated 10,460 are expected to die from the disease.2 While AML may occur at any age, adults at least 60 years of age are more likely than younger people to develop the disease.2 Although a substantial proportion of younger individuals who develop AML can be cured, AML in the elderly typically responds poorly to standard therapy with few complete remissions.

AML may develop from the progression of other diseases, such as MDS. MDS are a group of diverse bone marrow disorders in which the bone marrow does not produce enough healthy blood cells. MDS is often referred to as a "bone marrow failure disorder."

Novartis presents new data from large European study reinforcing the benefit of first-line Tasigna® in newly-diagnosed patients with CML

On June 13, 2015 Novartis reported long-term safety and efficacy results from the pivotal Phase III RESPONSE study evaluating Jakavi (ruxolitinib) for the treatment of patients with polycythemia vera (PV) who are resistant to or intolerant of hydroxyurea (Press release, Novartis, JUN 13, 2015, View Source [SID:1234505425]). A preplanned analysis of the study at 18 months demonstrated that 80% of patients with inadequately controlled PV treated with Jakavi experienced a durable response of sustaining hematocrit less than 45% without the use of phlebotomy and reducing spleen size, two key measures of disease control, for at least one year[1]. Findings were presented at the 20th Congress of the European Hematology Association (EHA) (Free EHA Whitepaper) in Vienna, Austria.

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"Polycythemia vera can lead to serious complications if inadequately controlled, and these data demonstrate the ability of Jakavi to provide a durable and comprehensive clinical benefit in this patient population," said lead study investigator Jean-Jacques Kiladjian, MD, PhD, Hôpital Saint-Louis et Université Paris Diderot. "There is currently a significant unmet need for patients with polycythemia vera who are unable to tolerate or control their disease on other treatments. For these patients, Jakavi represents a valuable new option as confirmed by results from the long-term Phase III study."

PV is a rare and incurable blood cancer associated with an overproduction of blood cells that can cause serious cardiovascular complications, such as blood clots, stroke and heart attack[3]. Approximately 25% of patients with PV develop resistance (inadequate response) to or intolerance (unacceptable side effects) of hydroxyurea and are considered to have inadequately controlled disease[2]. This is typically defined as hematocrit levels greater than 45%, elevated white blood cell count and/or platelet count, and may be accompanied by debilitating symptoms and/or an enlarged spleen[2],[4],[5].

In the Phase III study, 83% of patients with PV randomized to Jakavi were still receiving treatment at 18 months (median exposure of 111 weeks) compared to 0 patients on the best available treatment arm. Results also show that Jakavi-treated patients who achieved hematocrit control without phlebotomy had an 89% probability of maintaining their response for 18 months from the time of their initial response and all patients who had an initial spleen response maintained their reduction in spleen size. Of the patients on the Jakavi arm at week 32, 90% of patients did not have a phlebotomy between weeks 32 and 80. In addition, patients treated with Jakavi who achieved complete hematologic remission at week 32 had a 69% probability of maintaining their response for at least 18 months from the time of their initial response[1]. A separate analysis of the study at 18 months demonstrated treatment with Jakavi also led to sustained control of white blood cell and platelet levels, important PV hematologic parameters, with the largest reductions for patients with the most elevated values at baseline[6].

"Until the recent European Commission approval of Jakavi for the treatment of adult patients with polycythemia vera, there were limited alternative treatments available for these patients," said Bruno Strigini, President, Novartis Oncology. "These long-term data not only reinforce the robust evidence we have surrounding Jakavi in polycythemia vera, but also our commitment to bringing new and innovative therapies to people with blood cancers."

Overall, Jakavi was well tolerated. In the Jakavi-treatment arm, the rate for Grade 3 or 4 anemia and thrombocytopenia was 0.9 and 2.6 events per 100 patient-year exposure, respectively, and did not increase from the week 48 analysis. The most common non-hematologic adverse events (AEs) in the Jakavi arm were headache, diarrhea, pruritus and fatigue, which were mainly Grade 1 or 2. Treatment discontinuation due to AEs remained low in the Jakavi arm (4.5%)[1].

About the Pivotal Clinical Trial
RESPONSE is a global, randomized, open-label trial conducted at more than 90 trial sites. 222 patients with PV resistant to or intolerant of hydroxyurea were randomized 1:1 to receive either Jakavi (starting dose of 10 mg twice daily) or best available therapy, which was defined as investigator-selected monotherapy or observation only. The Jakavi dose was adjusted as needed throughout the trial. In the Jakavi arm, patients had a PV diagnosis for a median of 8.2 years and had previously received hydroxyurea for a median of approximately three years. Most patients (>80%) had received at least two phlebotomies in the last 24 weeks prior to screening. Patients were classified as intolerant or resistant to hydroxyurea based on the modified European LeukemiaNet (ELN) defined criteria[1].

The primary endpoint of the trial was the proportion of patients whose hematocrit was controlled without phlebotomy eligibility from week 8 through 32 (with no more than one phlebotomy eligibility between randomization and week 8) and whose spleen volume was reduced by 35% or more from baseline as assessed by imaging at week 32. Patients in the trial who were deemed to be eligible for phlebotomy had hematocrit that was greater than 45% and had increased three or more percentage points from the time they entered the trial (e.g., at baseline), or hematocrit greater than 48%. A second, preplanned analysis was performed at 80 weeks (18 months) evaluating durability of primary response, hematocrit control, spleen size reduction, complete hematologic remission and safety. Also at this 80 week data cutoff, a separate analysis evaluating hematologic parameters was assessed by baseline level[1].

About Polycythemia Vera
PV is a rare and incurable blood cancer associated with an overproduction of blood cells in the bone marrow that affects roughly one to three people per 100,000 globally[3],[7]. The disease is driven by the dysregulation of the JAK-STAT pathway[8]. It is typically characterized by elevated hematocrit, the volume percentage of red blood cells in whole blood, which can lead to a thickening of the blood and an increased risk of blood clots, as well as an elevated white blood cell and platelet count[3]. This can cause serious cardiovascular complications, such as stroke and heart attack, resulting in increased morbidity and mortality[9]. Additionally, patients with PV may have an enlarged spleen and symptoms that are frequent and burdensome, with an overall impact on quality of life similar to that seen with myelofibrosis[5],[10].

A common PV treatment includes phlebotomy, a procedure to remove blood from the body to reduce the concentration of red blood cells, which is used to help maintain a hematocrit level below 45%[3],[9]. However, phlebotomy is usually unsuitable as a permanent treatment option due to its inability to control symptoms or effectively manage the overproduction of red blood cells, therefore cytoreductive agents, such as hydroxyurea, may be added[9]. For patients requiring phlebotomy in combination with hydroxyurea, hematocrit may fluctuate and remain at unsafe levels for significant periods of time[11]. Unfortunately, approximately 25% of patients with PV become resistant to or intolerant of hydroxyurea treatment according to ELN criteria, resulting in inadequate disease control and an increased risk of progression[2].

About Jakavi
Jakavi (ruxolitinib) is an oral inhibitor of the JAK 1 and JAK 2 tyrosine kinases. Jakavi is approved by the European Commission for the treatment of adult patients with polycythemia vera (PV) who are resistant to or intolerant of hydroxyurea and for the treatment of disease-related splenomegaly or symptoms in adult patients with primary myelofibrosis (also known as chronic idiopathic myelofibrosis), post-polycythemia vera myelofibrosis or post-essential thrombocythemia myelofibrosis. Jakavi is approved in more than 80 countries for patients with myelofibrosis, including countries in the European Union, Canada, Japan and countries in Asia, Latin and South America. Additional worldwide regulatory filings are underway in myelofibrosis and PV.

Novartis licensed ruxolitinib from Incyte Corporation for development and commercialization outside the United States. Jakavi is marketed in the United States by Incyte Corporation as Jakafi for the treatment of patients with PV who have had an inadequate response to or are intolerant of hydroxyurea and for the treatment of patients with intermediate or high-risk myelofibrosis.

The recommended starting dose of Jakavi in PV is 10 mg given orally twice daily. The recommended starting dose of Jakavi in myelofibrosis is 15 mg twice daily for patients with a platelet count between 100,000 cubic millimeters (mm3) and 200,000 mm3, and 20 mg twice daily for patients with a platelet count of >200,000 mm3. Doses may be titrated based on safety and efficacy. There is limited information to recommend a starting dose for myelofibrosis and PV patients with platelet counts between 50,000/mm3 and <100,000/mm3. The maximum recommended starting dose in these patients is 5 mg twice daily, and patients should be titrated cautiously[12].

Jakavi is a registered trademark of Novartis AG in countries outside the United States. Jakafi is a registered trademark of Incyte Corporation. The safety and efficacy profile of Jakavi has not yet been established outside the approved indications.

Jakavi Important Safety Information for Treatment of Myelofibrosis (MF) and Polycythemia Vera (PV)
Jakavi can cause serious side effects, including a decrease in blood cell count and infections. Complete blood count monitoring is recommended. Dose reduction or interruption may be required in patients with any hepatic impairment or severe renal impairment or in patients developing hematologic adverse reactions such as thrombocytopenia, anemia and neutropenia. Dose reductions are also recommended when Jakavi is co-administered with strong CYP3A4 inhibitors or fluconazole. Use of Jakavi during pregnancy is not recommended, and women should avoid becoming pregnant during Jakavi therapy. Women taking Jakavi should not breast feed. Progressive multifocal leukoencephalopathy (PML) has been reported. Physicians should be alert for neuropsychiatric symptoms suggestive of PML. Hepatitis B viral load (HBV-DNA titer) increases have been reported in patients with chronic HBV infections. Patients with chronic HBV infection should be treated and monitored according to clinical guidelines. Non-melanoma skin cancer (NMSC) has been reported in Jakavi treated patients. Periodic skin examination is recommended. Very common adverse reactions in MF (>10%) include urinary tract infections, anemia, thrombocytopenia, neutropenia, hypercholesterolemia, dizziness, headache, alanine aminotransferase increased, aspartate aminotransferase increased, bruising and weight gain. Common adverse reactions in MF (1 to 10%) include herpes zoster and flatulence. Uncommon adverse reactions in MF include tuberculosis. Very common adverse reactions in PV (>10%) include anemia, thrombocytopenia, hypercholesterolemia, hypertriglyceridemia, dizziness, alanine aminotransferase increased and aspartate aminotransferase increased. Common adverse reactions in PV (1 to 10%) include urinary tract infections, herpes zoster, weight gain, constipation and hypertension.