AC Immune Receives Milestone Payment in Connection with Initiation of a Phase 2 Trial of Tau PET Tracer PI-2620

On September 17, 2019 AC Immune SA (NASDAQ: ACIU), a Swiss-based, clinical-stage biopharmaceutical company with a broad pipeline focused on neurodegenerative diseases, reported it has received a milestone payment from its partner Life Molecular Imaging in connection with the initiation of a Phase 2 study of the Tau positron-emission tomography (PET) tracer PI-2620 (Press release, AC Immune, SEP 17, 2019, View Source [SID1234539581]).

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PI-2620 is a next generation Tau PET tracer developed using AC Immune’s proprietary Morphomer discovery platform in a research collaboration with Life Molecular Imaging. It binds to Tau deposits which, along with beta-amyloid plaques, represent a critical pathological hallmark of Alzheimer’s disease (AD). Tau deposits also play an important role in other neurodegenerative diseases.

The Phase 2 longitudinal study is being conducted in the UK and is expected to last approximately three years, with the overall goal being to evaluate PI-2620 as a targeted radiopharmaceutical for the detection of Tau deposits in the human brain. The data generated are intended to be used for obtaining regulatory approval in the U.S. and Europe.

Prof. Andrea Pfeifer, CEO of AC Immune SA, commented: "The clinical advancement of PI-2620 is based on its excellent properties and imaging characteristics, and it further reinforces the proficiency of AC Immune’s Morphomer technology and our ability to establish highly productive partnerships with well-respected companies such as Life Molecular Imaging. Treating earlier and targeting Tau are both key elements of our Roadmap to Successful Therapies for Neurodegenerative Diseases.

"There is a growing body of clinical evidence that Tau pathology drives disease progression, and this new Phase 2 trial further broadens AC Immune’s world leading anti-Tau clinical pipeline, which also includes therapeutic antibodies (partnered with Roche/Genentech), small molecule inhibitors (partnered with Eli Lilly), and vaccines (partnered with Janssen). We are advancing these programs in parallel to generate robust clinical data, having most recently vaccinated the first patient in a Phase 1b/2a study of our clinically advanced anti-phospho-Tau vaccine candidate ACI-35.030."

The open label Phase 2 study will evaluate the safety and imaging characteristics of PI-2620 as a PET radioligand for imaging Tau deposition in the brains of patients with mild cognitive impairment (MCI) and mild to moderate AD in comparison with non-demented control (NDC) participants.

PI-2620 was discovered and developed in a research collaboration between AC Immune and Life Molecular Imaging. It has demonstrated robust brain uptake and fast wash-out in non-target regions, a broad imaging window between 30 and 90 minutes post-injection (p.i.) for AD, and excellent reproducibility between test and retest scans. The absence of significant off-target binding enables PI-2620 to detect and quantify early Tau deposition in the brain. PI-2620 also shows promise for non-AD Tauopathies like progressive supranuclear palsy (PSP). Life Molecular Imaging has the exclusive, worldwide license for research, development and commercialization of Tau PET tracers generated within the discovery program.

REVOLUTION Medicines Announces Dosing of First Patient in RMC-4630-02, a Phase 1b/2 Trial Combining RMC-4630 with a MEK Inhibitor

On September 17, 2019 REVOLUTION Medicines, Inc., a clinical-stage oncology company focused on developing novel targeted therapies to inhibit elusive frontier targets within notorious cancer pathways, reported dosing of the first patient in an open-label, Phase 1b/2 dose-escalation and dose-expansion study of RMC-4630 in combination with cobimetinib (Cotellic) in patients with relapsed/refractory solid tumors harboring specific genomic mutations (Press release, Revolution Medicines, SEP 17, 2019, View Source [SID1234539598]). RMC-4630, a SHP2 inhibitor, and Cotellic, a MEK inhibitor, are selective inhibitors of oncogenic targets at distinct positions within the RAS signaling cascade that is frequently exploited by human cancers and may develop adaptive resistance to single agent treatment. A combination of these complementary mechanisms of action demonstrated synergistic anti-tumor effects in preclinical cancer models carrying select oncogenic mutations of RAS or associated proteins. These findings provide a compelling scientific rationale to explore the potential of this combination regimen in patients with tumors driven by such mutations.

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RMC-4630 is a potent and orally bioavailable small molecule that selectively inhibits the activity of SHP2, an upstream cellular protein that plays a key role in modulating cell growth by transmitting signals from receptor tyrosine kinases to RAS. RMC-4630 and SHP2 are the focus of an exclusive global research, development and commercialization agreement with Sanofi. Cobimetinib, marketed in the U.S. by Genentech, a member of the Roche group, selectively inhibits the activity of MEK, a downstream effector of RAS that affects cell survival and growth. Under a clinical collaboration agreement, Genentech is providing cobimetinib for the combination study being conducted by REVOLUTION Medicines.

"Preclinical and clinical research have clearly established that oncogenic signaling involving RAS can exploit multiple cellular mechanisms to overcome therapeutic inhibition of individual pathway targets. We believe that rationally designed drug combinations inhibiting multiple nodes within the pathway may provide an effective strategy for defeating these inherent resistance mechanisms," said Mark A. Goldsmith, M.D., Ph.D., president and chief executive officer of REVOLUTION Medicines. "While we continue studying RMC-4630 as a single agent in our first clinical study, RMC-4630-01, we are also evaluating its effects in combination with a MEK inhibitor in this second study, RMC-4630-02."

The Phase 1b/2 RMC-4630-02 study will evaluate the safety, tolerability, pharmacokinetic, and pharmacodynamic profiles of RMC-4630 and cobimetinib in adult patients with relapsed/refractory solid tumors that harbor specific genomic mutations. The trial will seek to identify the maximum tolerated dose of RMC-4630 in combination with cobimetinib as well as the recommended dose for a subsequent Phase 2 trial of the combination.

Cobimetinib is approved in the U.S. for the treatment of patients with BRAFV600E or BRAFV600K mutation-positive unresectable or metastatic melanoma in combination with vemurafenib (Zelboraf).

About RMC-4630 and Sanofi Collaboration

RMC-4630 is currently being evaluated in a Phase 1 monotherapy clinical trial (RMC-4630-01) for a range of tumor types featuring specific, molecularly-defined oncogenic mutations, as well as a Phase 1b/2 study (RMC-4630-02) in combination with cobimetinib in patients with relapsed/refractory solid tumors displaying specific genomic mutations. The RMC-4630 program is the focus of an exclusive global research, development and commercialization agreement with Sanofi, under which REVOLUTION Medicines received a $50 million upfront payment, and Sanofi will cover research and development costs for the joint SHP2 program. Sanofi received an exclusive worldwide license for global commercialization of any approved products targeting SHP2, subject to a U.S. co-promote right for REVOLUTION Medicines. The companies will enter into a 50/50 profit and loss share arrangement in the U.S., and REVOLUTION Medicines will receive a tiered royalty reaching mid-double digits on sales in other markets. REVOLUTION Medicines could also receive more than $500 million in development and regulatory milestone payments.

Oncolytics Biotech to Present at the Ladenburg Thalmann Healthcare Conference

On September 17, 2019 Oncolytics Biotech Inc. (NASDAQ:ONCY) (TSX:ONC), currently developing pelareorep, an intravenously delivered immuno-oncolytic virus, reported that Matt Coffey, President & CEO of Oncolytics Biotech, will present at the Ladenburg Thalmann Healthcare Conference at 11:00 am Eastern Time on Tuesday, September 24, 2019 (Press release, Oncolytics Biotech, SEP 17, 2019, View Source [SID1234539582]). The conference is being held on September 24, 2019 at the Hotel Sofitel in New York City.

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A live audio link to the webcast session will be available on the Company’s website at View Source It is recommended that listeners log on 10 minutes in advance of the live session to register and download any necessary software. An audio replay will be accessible approximately two hours following the presentation on the Oncolytics website.

Janssen to Highlight Depth of Prostate Cancer and Solid Tumor Portfolios with Multiple Data Presentations at ESMO 2019

On September 17, 2019 The Janssen Pharmaceutical Companies of Johnson & Johnson reported multiple data presentations from its prostate cancer and solid tumor portfolios will be featured at the European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) Annual Congress 2019, taking place September 27 to October 1 in Barcelona, Spain (Press release, Johnson & Johnson, SEP 17, 2019, View Source [SID1234539599]). Among Janssen’s 12 accepted abstracts are an oral presentation reporting updated overall survival results from the ERLEADA (apalutamide) Phase 3 SPARTAN study in patients with non-metastatic castration-resistant prostate cancer (nmCRPC); patient-reported outcomes from the ERLEADA Phase 3 TITAN study in patients with metastatic castration-sensitive prostate cancer (mCSPC), demonstrating preservation of overall health-related quality of life; and a late-breaking interim analysis from the Phase 2 GALAHAD study evaluating niraparib in the treatment of patients with metastatic castration-resistant prostate cancer (mCRPC) and biallelic DNA-repair gene defects (DRD).

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"Janssen is focused on addressing areas of unmet need in both prostate cancer and solid tumors, and this year’s ESMO (Free ESMO Whitepaper) Annual Congress provides an opportunity to share these important study results for both approved and investigational therapies," said Mark Wildgust, Ph.D., Vice President, Global Medical Affairs, Oncology, Janssen Research & Development, LLC. "In particular, we look forward to presenting new data for ERLEADA and niraparib, which reinforce our continued commitment to improve outcomes for patients diagnosed with prostate cancer across the disease spectrum."

Company-sponsored abstracts to be presented at the meeting include:

Abstract No.

Title

Date/Time

ERLEADA (apalutamide)

Oral Presentation

Abstract #843O

Apalutamide and Overall Survival in Patients with Nonmetastatic Castration-Resistant Prostate Cancer (nmCRPC): Updated Results from the Phase 3 SPARTAN Study

Friday,
September 27
2:39 PM – 2:51 PM CET

Poster Presentations

Abstract #851PD

Patient-Reported Outcomes (PROs) From TITAN: A Phase 3, Randomized, Double-Blind Study of Apalutamide Versus Placebo

Added to Androgen Deprivation Therapy in Patients with Metastatic Castration-Sensitive Prostate Cancer (mCSPC)

Monday, September 30

12:00 PM CET

Abstract #883P

Androgen Receptor Aberrations in Patients with Metastatic Castration-Sensitive Prostate Cancer (mCSPC) Treated with Apalutamide Plus Androgen Deprivation Therapy in TITAN

Monday, September 30

12:00 PM CET

Abstract #900TiP

A Phase 2 randomized, open-label study comparing salvage radiotherapy in combination with 6 months of androgen-deprivation therapy with LHRH agonist or antagonist versus anti-androgen therapy with apalutamide in patients with biochemical progression after radical prostatectomy

Monday, September 30

12:00 PM CET

Niraparib

Poster Presentations

Abstract #LBA50

Pre-specified interim analysis of GALAHAD: A Phase 2 study of niraparib in patients with metastatic castration-resistant prostate cancer (mCRPC) and biallelic DNA-repair gene defects

Sunday, September 29

8:30 AM CET

Abstract #897TiP

A Phase 3 randomized, placebo-controlled, double-blind study of niraparib plus abiraterone acetate and prednisone versus abiraterone acetate and prednisone in patients with metastatic prostate cancer (NCT03748641)

Monday, September 30

12:00 PM CET

Abstract #1412P

Analytical performance of the Resolution-HRD plasma assay used to identify mCRPC patients with biallelic disruption of DNA repair genes for treatment with niraparib

Monday, September 30

12:00 PM CET

ZYTIGA (abiraterone acetate)

Poster Presentation

Abstract #95P

Evaluation of markers associated with efficacy of abiraterone acetate plus prednisone in patients with castration-sensitive prostate cancer (mCSPC) from the LATITUDE study

Monday, September 30

12:00 PM CET

BALVERSA (erdafitinib)

Poster Presentations

Abstract #925P

Analysis of response to prior therapies and therapies after treatment with erdafitinib in fibroblast growth factor receptor (FGFR)-positive patients with metastatic urothelial carcinoma

Monday, September 30

12:00 PM CET

Abstract #926P

Erdafitinib versus available therapies in advanced urothelial cancer: A matching adjusted indirect comparison

Monday, September 30

12:00 PM CET

Abstract #932P

Hyperphosphatemia due to Erdafitinib (a Pan-FGFR Inhibitor) and Antitumor Activity Among Patients with Advanced Urothelial Carcinoma

Monday, September 30

12:00 PM CET

Solid Tumor Portfolio

Poster Presentation

Abstract #488P

Correlation of Progression Free Survival-2 and Overall Survival in Solid Tumors

Saturday, September 28

2:00 PM CET

About ERLEADA (apalutamide)
ERLEADA (apalutamide) is an androgen receptor (AR) inhibitor indicated for the treatment of patients with nmCRPC.1 It became the first treatment to receive FDA approval for nmCRPC on February 14, 2018.1 ERLEADA was also approved for the treatment of nmCRPC by the European Commission on January 12, 2019. ERLEADA is being studied in five Phase 3 registrational clinical trials. The NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Prostate Cancer include apalutamide as a treatment option for patients with non-metastatic (M0) CRPC with a category 1 recommendation for those with a PSA doubling time ≤10 months*.2 Similarly, the American Urological Association (AUA) Guidelines for Castration-Resistant Prostate Cancer (CRPC) recommend clinicians offer apalutamide (ERLEADA) with continued androgen deprivation therapy (ADT) as one of the treatment options for patients with nmCRPC at high risk for developing metastatic disease. (Standard; Evidence Level Grade A)**.3 ERLEADA is taken orally, once daily, with or without food.1

*Referenced from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines) for Prostate Cancer V.4.2019. © National Comprehensive Cancer Network, Inc. 2019. All rights reserved. Accessed September 5, 2019. To view the most recent and complete version of the NCCN Guidelines, go online to NCCN.org. NCCN makes no warranties of any kind whatsoever regarding their content, use, or application, and disclaims any responsibility for their application or use in any way

**Standard: Directive statement that an action should (benefits outweigh risks/burdens) or should not (risks/burdens outweigh benefits) be taken based on Grade A or B evidence.

**Evidence Level: A designation indicating the certainty of the results as high, moderate, or low (A, B, or C, respectively) based on AUA nomenclature and methodology.

About Niraparib
Niraparib is an orally-administered selective poly ADP ribose polymerase (PARP) inhibitor that is currently being studied by Janssen for the treatment of patients with prostate cancer. In April 2016, Janssen entered a worldwide (except Japan) collaboration and license agreement with TESARO, Inc., for exclusive rights to niraparib in prostate cancer. In the U.S., niraparib is indicated for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in a complete or partial response to platinum-based chemotherapy.4 Niraparib is currently marketed as ZEJULA by TESARO, an oncology-focused business within GSK, devoted to providing transformative therapies to people facing cancer. Please refer to the full Prescribing Information available at View Source

About ZYTIGA (abiraterone acetate)
ZYTIGA (abiraterone acetate) in combination with prednisone is indicated for the treatment of patients with metastatic castration-resistant prostate cancer (mCRPC), approved by the U.S. FDA on April 28, 2011 and by the European Commission on September 7, 2011. Additionally, ZYTIGA was approved for the treatment of high-risk metastatic castration-sensitive prostate cancer (mCSPC) by the European Commission on November 20, 2017 and by the U.S. FDA on February 8, 2018. Since its first approval in the U.S. in 2011, ZYTIGA has been approved in combination with prednisone or prednisolone, in more than 100 countries. More than 500,000 patients worldwide have been prescribed ZYTIGA.

About BALVERSATM (erdafitinib)
BALVERSA (erdafitinib) is a once-daily, oral fibroblast growth factor receptor (FGFR) kinase inhibitor indicated for the treatment of adults with locally advanced or metastatic urothelial carcinoma (mUC) that has susceptible FGFR3 or FGFR2 genetic alterations and who have progressed during or following at least one line of prior platinum-containing chemotherapy, including within 12 months of neoadjuvant or adjuvant platinum-containing chemotherapy.5 In 2008, Janssen entered into an exclusive worldwide license and collaboration agreement with Astex Pharmaceuticals to develop and commercialize BALVERSA. This indication was approved by the U.S. FDA on April 12, 2019 under an accelerated approval based on tumor response rate. Patients may be suitable for BALVERSA based on an FDA-approved companion diagnostic. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials.4

For more information about BALVERSA, visit www.BALVERSA.com.

ERLEADA IMPORTANT SAFETY INFORMATION
CONTRAINDICATIONS

Pregnancy — ERLEADA (apalutamide) can cause fetal harm and potential loss of pregnancy.

WARNINGS AND PRECAUTIONS

Falls and Fractures — In a randomized study (SPARTAN), falls and fractures occurred in 16% and 12% of patients treated with ERLEADA compared to 9% and 7% treated with placebo, respectively. Falls were not associated with loss of consciousness or seizure. Evaluate patients for fracture and fall risk. Monitor and manage patients at risk for fractures according to established treatment guidelines and consider use of bone targeted agents.

Seizure — In a randomized study (SPARTAN), 2 patients (0.2%) treated with ERLEADA experienced a seizure. Permanently discontinue ERLEADA in patients who develop a seizure during treatment. It is unknown whether anti-epileptic medications will prevent seizures with ERLEADA. Advise patients of the risk of developing a seizure while receiving ERLEADA and of engaging in any activity where sudden loss of consciousness could cause harm to themselves or others.

ADVERSE REACTIONS

Adverse Reactions — The most common adverse reactions (≥10%) were fatigue, hypertension, rash, diarrhea, nausea, weight decreased, arthralgia, fall, hot flush, decreased appetite, fracture, and peripheral edema.

Laboratory Abnormalities — All Grades (Grade 3-4)

Hematology — anemia ERLEADA 70% (0.4%), placebo 64% (0.5%); leukopenia ERLEADA 47% (0.3%), placebo 29% (0%); lymphopenia ERLEADA 41% (2%), placebo 21% (2%)
Chemistry — hypercholesterolemia ERLEADA 76% (0.1%), placebo 46% (0%); hyperglycemia ERLEADA 70% (2%), placebo 59% (1%); hypertriglyceridemia ERLEADA 67% (2%), placebo 49% (0.8%); hyperkalemia ERLEADA 32% (2%), placebo 22% (0.5%)
Rash — Rash was most commonly described as macular or maculo-papular. Adverse reactions were 24% with ERLEADA versus 6% with placebo. Grade 3 rashes (defined as covering > 30% body surface area [BSA]) were reported with ERLEADA treatment (5%) versus placebo (0.3%).

The onset of rash occurred at a median of 82 days. Rash resolved in 81% of patients within a median of 60 days (range: 2 to 709 days) from onset of rash. Four percent of patients treated with ERLEADA received systemic corticosteroids. Rash recurred in approximately half of patients who were re-challenged with ERLEADA.

Hypothyroidism was reported for 8% of patients treated with ERLEADA and 2% of patients treated with placebo based on assessments of thyroid-stimulating hormone (TSH) every 4 months. Elevated TSH occurred in 25% of patients treated with ERLEADA and 7% of patients treated with placebo. The median onset was day 113. There were no Grade 3 or 4 adverse reactions. Thyroid replacement therapy, when clinically indicated, should be initiated or dose-adjusted.

DRUG INTERACTIONS

Effect of Other Drugs on ERLEADA — Co-administration of a strong CYP2C8 or CYP3A4 inhibitor is predicted to increase the steady-state exposure of the active moieties. No initial dose adjustment is necessary; however, reduce the ERLEADA dose based on tolerability [see Dosage and Administration (2.2)].

Effect of ERLEADA on Other Drugs — ERLEADA is a strong inducer of CYP3A4 and CYP2C19, and a weak inducer of CYP2C9 in humans. Concomitant use of ERLEADA with medications that are primarily metabolized by CYP3A4, CYP2C19, or CYP2C9 can result in lower exposure to these medications. Substitution for these medications is recommended when possible or evaluate for loss of activity if medication is continued. Concomitant administration of ERLEADA with medications that are substrates of UDP-glucuronosyl transferase (UGT) can result in decreased exposure. Use caution if substrates of UGT must be co-administered with ERLEADA and evaluate for loss of activity.

P-gp, BCRP or OATP1B1 substrates — Apalutamide is a weak inducer of P-glycoprotein (P- gp), breast cancer resistance protein (BCRP), and organic anion transporting polypeptide 1B1 (OATP1B1) clinically. Concomitant use of ERLEADA with medications that are substrates of P-gp, BCRP, or OATP1B1 can result in lower exposure of these medications. Use caution if substrates of P-gp, BCRP or OATP1B1 must be co-administered with ERLEADA and evaluate for loss of activity if medication is continued.

Please see the full Prescribing Information for ERLEADA.

ZYTIGA IMPORTANT SAFETY INFORMATION

WARNINGS AND PRECAUTIONS

Hypokalemia, Fluid Retention, and Cardiovascular Adverse Reactions due to Mineralocorticoid Excess – ZYTIGA may cause hypertension, hypokalemia, and fluid retention as a consequence of increased mineralocorticoid levels resulting from CYP17 inhibition [see Clinical Pharmacology (12.1)]. Monitor patients for hypertension, hypokalemia, and fluid retention at least once a month. Control hypertension and correct hypokalemia before and during treatment.

Closely monitor patients whose underlying medical conditions might be compromised by increases in blood pressure, hypokalemia, or fluid retention, such as those with heart failure, recent myocardial infarction, cardiovascular disease, or ventricular arrhythmia. In postmarketing experience, QT prolongation, and torsades de pointes have been observed in patients who develop hypokalemia while taking ZYTIGA. The safety of ZYTIGA in patients with left ventricular ejection fraction <50% or New York Heart Association (NYHA) Class III or IV heart failure (in COU-AA-301) or NYHA Class II to IV heart failure (in COU-AA-302 and LATITUDE) has not been established because these patients were excluded from these randomized clinical trials [see Clinical Studies (14)].

Adrenocortical Insufficiency – Adrenocortical insufficiency was reported in patients receiving ZYTIGA in combination with prednisone, after an interruption of daily steroids and/or with concurrent infection or stress. Monitor patients for symptoms and signs of adrenocortical insufficiency if prednisone is stopped or withdrawn, if the prednisone dose is reduced, or if the patient experiences unusual stress. Symptoms and signs of adrenocortical insufficiency may be masked by adverse reactions associated with mineralocorticoid excess seen in patients treated with ZYTIGA. Perform appropriate tests, if clinically indicated, to confirm adrenocortical insufficiency. Increased dosages of corticosteroids may be used before, during, and after stressful situations [see Warnings and Precautions (5.1)].

Hepatotoxicity – In postmarketing experience, there have been ZYTIGA-associated severe hepatic toxicities, including fulminant hepatitis, acute liver failure, and deaths. Measure serum transaminases (ALT and AST) and bilirubin levels prior to starting treatment with ZYTIGA, every two weeks for the first three months of treatment, and monthly thereafter. In patients with baseline moderate hepatic impairment receiving a reduced ZYTIGA dose of 250 mg, measure ALT, AST, and bilirubin prior to the start of treatment, every week for the first month, every two weeks for the following two months of treatment, and monthly thereafter. Promptly measure serum total bilirubin, AST, and ALT if clinical symptoms or signs suggestive of hepatotoxicity develop. Elevations of AST, ALT, or bilirubin from the patient’s baseline should prompt more frequent monitoring. If at any time AST or ALT rise above five times the upper limit of normal (ULN) or the bilirubin rises above three times the ULN, interrupt ZYTIGA treatment and closely monitor liver function. Re-treatment with ZYTIGA at a reduced dose level may take place only after return of liver function tests to the patient’s baseline or to AST and ALT less than or equal to 2.5X ULN and total bilirubin less than or equal to 1.5X ULN [see Dosage and Administration (2.4)].

Permanently discontinue ZYTIGA for patients who develop a concurrent elevation of ALT greater than 3X ULN and total bilirubin greater than 2X ULN in the absence of biliary obstruction or other causes responsible for the concurrent elevation.

The safety of ZYTIGA re-treatment of patients who develop AST or ALT greater than or equal to 20X ULN and/or bilirubin greater than or equal to 10X ULN is unknown.

Increased Fractures and Mortality in Combination with Radium Ra 223 Dichloride – ZYTIGA plus prednisone/prednisolone is not recommended for use in combination with radium Ra 223 dichloride outside of clinical trials. Increased incidences of fractures (28.6% vs 11.4%) and deaths (38.5% vs 35.5%) have been observed in patients who received ZYTIGA plus prednisone/prednisolone in combination with radium Ra 223 dichloride compared to patients who received placebo in combination with ZYTIGA plus prednisone/prednisolone [see Warnings and Precautions (5.4)].

Embryo-Fetal Toxicity – The safety and efficacy of ZYTIGA have not been established in females. Based on animal reproductive studies and mechanism of action, ZYTIGA can cause fetal harm and loss of pregnancy when administered to a pregnant female. Advise males with female partners of reproductive potential to use effective contraception during treatment with ZYTIGA and for 3 weeks after the last dose of ZYTIGA [see Use in Specific Populations (8.1, 8.3)]. ZYTIGA should not be handled by females who are or may become pregnant [see How Supplied/Storage and Handling (16)].

ADVERSE REACTIONS

Adverse Reactions – The most common adverse reactions (≥10%) are fatigue, arthralgia, hypertension, nausea, edema, hypokalemia, hot flush, diarrhea, vomiting, upper respiratory tract infection, cough, and headache.

The most common laboratory abnormalities (>20%) are anemia, elevated alkaline phosphatase, hypertriglyceridemia, lymphopenia, hypercholesterolemia, hyperglycemia, and hypokalemia.

Drug Interactions – Based on in vitro data, ZYTIGA is a substrate of CYP3A4. In a drug interaction trial, co-administration of rifampin, a strong CYP3A4 inducer, decreased exposure of abiraterone by 55%. Avoid concomitant strong CYP3A4 inducers during ZYTIGA treatment. If a strong CYP3A4 inducer must be co-administered, increase the ZYTIGA dosing frequency only during the co-administration period [see Dosage and Administration (2.3)]. In a dedicated drug interaction trial, co-administration of ketoconazole, a strong inhibitor of CYP3A4, had no clinically meaningful effect on the pharmacokinetics of abiraterone.

ZYTIGA is an inhibitor of the hepatic drug-metabolizing enzymes CYP2D6 and CYP2C8. Avoid co-administration with CYP2D6 substrates with a narrow therapeutic index. If alternative treatments cannot be used, consider a dose reduction of the CYP2D6 substrate drug. In a CYP2C8 drug interaction trial in healthy subjects, the AUC of pioglitazone, a CYP2C8 substrate, was increased by 46% when administered with a single dose of ZYTIGA. Patients should be monitored closely for signs of toxicity related to a CYP2C8 substrate with a narrow therapeutic index if used concomitantly with ZYTIGA.

Use in Specific Populations –

Females and Males of Reproductive Potential: Advise males with female partners of reproductive potential to use effective contraception.
Do not use ZYTIGA in patients with baseline severe hepatic impairment (Child-Pugh Class C).
Please read the full Prescribing Information and Patient Information for ZYTIGA.

BALVERSA IMPORTANT SAFETY INFORMATION
Ocular Disorders – BALVERSATM can cause ocular disorders, including central serous retinopathy/retinal pigment epithelial detachment (CSR/RPED) resulting in visual field defect.

CSR/RPED was reported in 25% of patients treated with BALVERSATM, with a median time to first onset of 50 days. Grade 3 CSR/RPED, involving central field of vision, was reported in 3% of patients. CSR/RPED resolved in 13% of patients and was ongoing in 13% of patients at the study cutoff. CSR/RPED led to dose interruptions and reductions in 9% and 14% of patients, respectively and 3% of patients discontinued BALVERSATM. Dry eye symptoms occurred in 28% of patients during treatment with BALVERSATM and were Grade 3 in 6% of patients. All patients should receive dry eye prophylaxis with ocular demulcents as needed.

Perform monthly ophthalmological examinations during the first 4 months of treatment and every 3 months afterwards, and urgently at any time for visual symptoms. Ophthalmological examination should include assessment of visual acuity, slit lamp examination, fundoscopy, and optical coherence tomography. Withhold BALVERSATM when CSR occurs and permanently discontinue if it does not resolve within 4 weeks or if Grade 4 in severity. For ocular adverse reactions, follow the dose modification guidelines [see Dosage and Administration (2.3)].

Hyperphosphatemia – Increases in phosphate levels are a pharmacodynamic effect of BALVERSA [see Pharmacodynamics (12.2)]. Hyperphosphatemia was reported as adverse reaction in 76% of patients treated with BALVERSA. The median onset time for any grade event of hyperphosphatemia was 20 days (range: 8-116) after initiating BALVERSA. Thirty-two percent of patients received phosphate binders during treatment with BALVERSA. Monitor for hyperphosphatemia and follow the dose modification guidelines when required [see Dosage and Administration (2.2, 2.3)].

Embryo-fetal Toxicity – Based on the mechanism of action and findings in animal reproduction studies, BALVERSA can cause fetal harm when administered to a pregnant woman. In a rat embryo-fetal toxicity study, erdafitinib was embryotoxic and teratogenic at exposures less than the human exposures at all doses studied. Advise pregnant women of the potential risk to the fetus. Advise female patients of reproductive potential to use effective contraception prior to and during treatment, and for one month after the last dose. Advise male patients with female partners of reproductive potential to use effective contraception during treatment with BALVERSA and for one month after the last dose [see Use in Specific Populations (8.1, 8.3) and Clinical Pharmacology (12.1)].

Most common adverse reactions including laboratory abnormalities > 20% were: Phosphate increased (76%), stomatitis (56%), fatigue (54%), creatinine increased (52%), diarrhea (47%), dry mouth (45%), onycholysis (41%), alanine aminotransferase increased (41%), alkaline phosphatase increased (41%), sodium decreased (40%), decreased appetite (38%), albumin decreased (37%), dysgeusia (37%), hemoglobin decreased (35%), dry skin (34%), aspartate aminotransferase increased (30%), magnesium decreased (30%), dry eye (28%), alopecia (26%), palmar-plantar erythrodysesthesia syndrome (26%), constipation (28%), phosphate decreased (24%), abdominal pain (23%), calcium increased (22%), nausea (21%), and musculoskeletal pain (20%). The most common Grade 3 or greater adverse reactions (>1%) were stomatitis (9%), nail dystrophy*, palmar-plantar erythrodysesthesia syndrome (6%), paronychia (3%), nail disorder*, keratitis†, onycholysis* (10%), and hyperphosphatemia.

*Included within onycholysis. ^Included within dry eye.

An adverse reaction with a fatal outcome in 1% of patients was acute myocardial infarction.

Serious adverse reactions occurred in 41% of patients, including eye disorders (10%).

Permanent discontinuation due to an adverse reaction occurred in 13% of patients. The most frequent reasons for permanent discontinuation included eye disorders (6%).

Dosage interruptions occurred in 68% of patients. The most frequent adverse reactions requiring dosage interruption included hyperphosphatemia (24%), stomatitis (17%), eye disorders (17%), and palmar-plantar erythrodysesthesia syndrome (8%).

Dose reductions occurred in 53% of patients. The most frequent adverse reactions for dose reductions included eye disorders (23%), stomatitis (15%), hyperphosphatemia (7%), palmar-plantar erythrodysesthesia syndrome (7%), paronychia (7%), and nail dystrophy (6%).

Drug Interactions

Strong CYP2C9 or CYP3A4 Inhibitors: Consider alternative agents or monitor closely for adverse reactions. (7.1)
Strong CYP2C9 or CYP3A4 inducers: Avoid concomitant use with BALVERSA. (7.1)
Moderate CYP2C9 or CYP3A4 inducers: Increase BALVERSA dose up to 9 mg. (7.1)
Serum phosphate level-altering agents: Avoid concomitant use with agents that can alter serum phosphate levels before the initial dose modification period. (2.3, 7.1)
CYP3A4 substrates: Avoid concomitant use with sensitive CYP3A4 substrates with narrow therapeutic indices. (7.2)
OCT2 substrates: Consider alternative agents or consider reducing the dose of OCT2 substrates based on tolerability. (7.2)
P-gp substrates: Separate BALVERSA administration by at least 6 hours before or after administration of P-gp substrates with narrow therapeutic indices. (7.2)
Use in Specific Populations
Lactation – Because of the potential for serious adverse reactions from erdafitinib in a breastfed child, advise lactating women not to breastfeed during treatment with BALVERSATM and for one month following the last dose.

Seattle Genetics Announces Presentations of New Clinical Data from Multiple Studies of Novel Targeted Therapies at the European Society for Medical Oncology (ESMO) 2019 Congress

On September 17, 2019 Seattle Genetics, Inc. (Nasdaq:SGEN) reported that new data from four of its investigational programs will be presented at the upcoming European Society for Medical Oncology (ESMO) (Free ESMO Whitepaper) 2019 Congress in Barcelona, Spain, from September 27 – October 1, 2019 (Press release, Seattle Genetics, SEP 17, 2019, View Source [SID1234539583]).

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"We look forward to the presentation featuring antibody-drug conjugate enfortumab vedotin in combination with the immune therapy pembrolizumab in patients with previously untreated advanced urothelial cancer," said Roger Dansey, M.D., Chief Medical Officer at Seattle Genetics. "We are also pleased to see initial results from an investigator-sponsored study called MOUNTAINEER examining the combination of our novel tyrosine kinase inhibitor tucatinib with trastuzumab for the treatment of HER2-amplified metastatic colorectal cancer. The development of these and other targeted medicines support our efforts toward becoming a multi-product oncology company."

Details of the oral presentation:

EV-103: Initial results of enfortumab vedotin plus pembrolizumab for locally advanced or metastatic urothelial carcinoma
Abstract: 901O
Presenter: C Hoimes, Case Western Reserve University, Cleveland, OH, USA
Session: Oral Presentation Proffered Paper Session – Genitourinary tumours, non-prostate
Date and Time: Saturday, September 28, 8:30-10:00 a.m. CEST
Location: Barcelona Auditorium, Hall 2

Details of company-sponsored presentations are as follows:

Systemic therapy in 2nd-line metastatic triple negative breast cancer (mTNBC): a systematic literature review (SLR) and meta-analysis (MA) of efficacy
Abstract: 360P
First Author: PA Kaufman, University of Vermont Cancer Center, Burlington, VT, USA
Session: Poster Presentation
Date and Time: Sunday, September 29, 12:00-1:00 p.m. CEST
Location: Barcelona Auditorium, Hall 4

Quality of life of metastatic urothelial cancer (mUC) patients treated with enfortumab vedotin (EV) following platinum-containing chemotherapy and a checkpoint inhibitor (CPI): data from EV-201 cohort 1
Abstract: 921P
First Author: B McGregor, Dana-Farber Cancer Institute, Boston, MA, USA
Session: Poster Presentation
Date and Time: Monday, September 30, 12:00-1:00 p.m. CEST
Location: Barcelona Auditorium, Hall 4

Phase 1/2 trial of tisotumab vedotin plus bevacizumab, pembrolizumab, or carboplatin in recurrent or metastatic cervical cancer (innovaTV 205/ENGOT-cx8)
Abstract: 1059TiP
First Author: I Vergote, Leuven Cancer Institute, Leuven, Belgium
Session: Poster Presentation
Date and Time: Sunday, September 29, 12:00-1:00 p.m. CEST
Location: Barcelona Auditorium, Hall 4

Details of select investigator-initiated trial presentation is as follows:

Trastuzumab and tucatinib for the treatment of HER2 amplified metastatic colorectal cancer (mCRC): Initial results from the MOUNTAINEER trial
Abstract: 527PD
First Author: JH Strickler, Duke University Medical Centre, Durham, NC, USA
Session: Poster Discussion Session – Gastrointestinal tumours, colorectal
Date and Time: Sunday, September 29, Poster Discussion: 3:00-3:15 p.m. CEST
Location: Cordoba Auditorium, Hall 7

For more information, including a complete list of abstract titles and presentation dates and times, visit the ESMO (Free ESMO Whitepaper) website at View Source

About Enfortumab Vedotin

Enfortumab vedotin is an investigational antibody-drug conjugate (ADC) composed of an anti-Nectin-4 monoclonal antibody attached to a microtubule-disrupting agent, MMAE, using Seattle Genetics’ proprietary linker technology. Enfortumab vedotin targets Nectin-4, a cell adhesion molecule that is expressed on many solid tumors, and that has been identified as an ADC target by Astellas. A Biologics License Application is currently under review by the U.S. Food and Drug Administration (FDA) for the treatment of patients with locally advanced or metastatic urothelial cancer who have received a PD-1/PD-L1 inhibitor and who have received a platinum-containing chemotherapy before (neoadjuvant) or after (adjuvant) surgery or in a locally advanced or metastatic setting. Enfortumab vedotin is being co-developed by Seattle Genetics and Astellas Pharma Inc.

The safety and efficacy of enfortumab vedotin are under investigation and have not been established. There is no guarantee that the agent will receive regulatory approval or become commercially available for the uses being investigated.

About Tisotumab Vedotin

Tisotumab vedotin is an antibody-drug conjugate (ADC) composed of Genmab’s human antibody that binds to Tissue Factor and Seattle Genetics’ ADC technology that utilizes a cleavable linker and the microtubule disrupting agent monomethyl auristatin E (MMAE). In cancer biology, Tissue Factor is a protein involved in tumor signaling and angiogenesis. The Tissue Factor antigen target is overexpressed in the vast majority of patients with cervical cancer and in many other solid tumors, including ovarian, lung, pancreatic, colorectal and head and neck. Based on its high expression on many solid tumors and its rapid internalization, Tissue Factor was selected as a target for an ADC approach. Tisotumab vedotin is being co-developed by Seattle Genetics and Genmab.

About Tucatinib

Tucatinib is an investigational, orally bioavailable, potent tyrosine kinase inhibitor that is highly selective for HER2 without significant inhibition of EGFR. Inhibition of EGFR has been associated with significant toxicities, including skin rash and diarrhea. Tucatinib has shown activity as a single agent and in combination with both chemotherapy and other HER2 directed agents such as trastuzumab.1 Studies of tucatinib in these combinations have shown activity both systemically and in brain metastases. 1 HER2 is a growth factor receptor that is overexpressed in multiple cancers, including breast, ovarian and gastric cancers. HER2 mediates cell growth, differentiation and survival. Tumors that overexpress HER2 are more aggressive and historically have been associated with poor overall survival compared with HER2-negative cancers. Tucatinib has been granted orphan drug designation by the FDA for the treatment of breast cancer patients with brain metastases.