On May 28, 2021 Halozyme Therapeutics, Inc. (NASDAQ: HALO) reported that it will participate at the following investor conferences (Press release, Halozyme, MAY 28, 2021, View Source [SID1234583267]):

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The Goldman Sachs 42nd Annual Global Healthcare Conference on Tuesday, June 8, 2021 at 11:20 a.m. ET / 8:20 a.m. ET. Dr. Helen Torley, president and chief executive officer, will represent the company in a fireside chat.
The JMP Securities Life Sciences Conference on Thursday, June 17, 2021 at 3:00 p.m. ET / 12:00 p.m. PT. Elaine Sun, senior vice president and chief financial officer, will represent the company in a fireside chat.
These conferences will be held virtually. Live webcasts of the applicable presentations will be accessible on the company’s website www.halozyme.com under the investors section and an archived recording will be available on the website for approximately one month following each presentation.

On May 28, 2021 Kuraray Group reported that FY2020 Earnings Announcement Presentation disclosed on February 10, 2021 (Press release, Kuraray, MAY 28, 2021, https://pdf.irpocket.com/C3405/M6bm/Wxzm/BKYp.pdf [SID1234583266]).

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1. Reason for correction
There was an error in the figures for CAPEX (Acceptance basis) for FY2020 in the sections on "Cash Flow for FY2020" (page 19) and "Forecast for FY2021" (page 22). There have been no changes to the previously disclosed Consolidated Financial Statements.

2. Correction details
Corrections have been made to the numbers circled in red.

On May 28, 2021 Novartis reported that it received approval from the US Food and Drug Administration (FDA) for the first targeted therapy for cancer, known as a tyrosine kinase inhibitor (TKI) (Press release, Novartis, MAY 28, 2021, View Source [SID1234583265]). This was a watershed moment in drug discovery, transforming the treatment landscape for chronic myeloid leukemia (CML), and opening the door to reimagining possibilities for other forms of cancer and blood disorders.

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The development of the first TKI was an unlikely success story. Back in the 1950s, scientists had a limited understanding of cancer, and specifically, how genes influence the disease. Nevertheless, research was intensified over the next few years, with hopes that the emerging understanding of genomics could bring forth lasting change. One particular gene, discovered by Drs Peter Nowell and David Hungerford from Philadelphia, was identified as a common factor in patients with CML. Soon after, it was learned that this gene, dubbed as the Philadelphia chromosome, was also the root cause of a faulty tyrosine kinase protein that was directly responsible for the blood cancer.

In the decades following Nowell and Hungerford’s discovery, Novartis had started to look more closely into this class of proteins. We collaborated with scientists and clinicians, including Dr Brian Druker, researcher at Oregon Health and Science University. It was Dr Druker who suggested that Novartis explore ways of developing a molecule with the ability to inhibit the faulty kinase – a drug that would target this disease trigger, different than the therapies available at that time. There was a pressing need; CML was a fatal disease and in the mid-1970s, the estimated five-year survival rate was only 22%.

I had one goal at the time – to find a company that had an inhibitor for BCR-ABL and to bring it into the clinic.

Brian Druker, MD, Director, Knight Cancer Institute at Oregon Health & Science University
What Came After
This milestone approval helped evolve treatment goals in CML and demonstrated Novartis’ commitment to research and innovation.

Looking Ahead: A bold Pursuit
Today, the five-year survival rate for patients with CML is estimated above 70%. Despite important advancements in CML care over the past 20 years, cancer and serious blood disorders are a devious enemy, and one breakthrough is not enough. Significant unmet needs still remain, particularly for patients in later lines of CML, who have experienced resistance or intolerance to available treatments. That’s why Novartis won’t stop in the continuous pursuit of bold science and striving to transform the lives of patients with CML.

At Novartis, we are relentless in the pursuit of cutting-edge medicines, from targeted therapies to treatments that harness the immune system and beyond. Like with CML, we must continue to take a bold approach with science to tackle some of the toughest-to-treat diseases and seek solutions for incredibly challenging public health issues facing our society today.

Novartis is a company for science and innovation. We have a big vision as a company, and that is to reimagine medicine – that is what we strive for. If you really want to change something, you must be bold and have the courage to take risks.

Susanne Schaffert, PhD, President of Novartis Oncology
With a heritage in developing transformative, first-in-class therapies for blood disorders, we open our minds to all scientific possibilities and reach further for new and different endpoints in hematologic diseases.

On May 28, 2021 BridgeBio Pharma, Inc. (Nasdaq: BBIO), through its affiliate QED Therapeutics, Inc., and Helsinn Group reported that the US Food and Drug Administration (FDA) has approved TRUSELTIQ (infigratinib) under the accelerated approval program for the treatment of patients with previously-treated locally advanced or metastatic cholangiocarcinoma (CCA) harboring an FGFR2 fusion or rearrangement (Press release, BridgeBio, MAY 28, 2021, View Source [SID1234583264]). TRUSELTIQ is an orally administered, ATP-competitive, tyrosine kinase inhibitor of FGFR. In the pivotal trial of patients with advanced, unresectable CCA, an aggressive malignancy with poor prognosis, TRUSELTIQ led to cases of tumor shrinkage. CCA is known to affect approximately 20,000 people in the United States and European Union each year and has a median five-year survival rate of only 9%.1

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"This is an important milestone for patients diagnosed with FGFR2-fusion-driven cholangiocarcinoma who have recurred after first-line therapy and are in need of targeted options for further treatment," said Susan Moran, M.D., M.S.C.E., Chief Medical Officer for QED. "Based on the efficacy seen to date, our team believes infigratinib possesses promise for a range of FGFR-driven conditions, including other cancers. We will continue to evaluate its safety and efficacy in these areas of unmet need."

The approval of TRUSELTIQ is based on a Phase 2 clinical study in which 108 patients who had undergone at least one prior treatment for advanced CCA received 125 mg of TRUSELTIQ daily for 21 days of 28-day cycles. Of these patients, 107 (99%) had Stage IV CCA. All patients had received at least 1 prior line of systemic therapy. The study’s primary endpoint demonstrated a confirmed objective response rate (ORR) of 23% (95% CI 16-32%). The study also showed a median duration of response (DOR) of 5.0 months (95% CI 3.7–9.3 months). Common adverse reactions and laboratory abnormalities (of >30%) were increased creatinine, increased phosphate, decreased phosphate, nail toxicity, stomatitis, increased alkaline phosphatase, decreased hemoglobin, increased alanine aminotransferase, dry eye, fatigue, increased lipase, decreased lymphocytes, increased calcium, decreased sodium, alopecia, increased triglycerides, increased aspartate aminotransferase, decreased platelets, increased urate, palmar-plantar erythrodysesthesia syndrome, arthralgia, and dysgeusia. Please see below for additional important safety information for TRUSELTIQ.

The above data were presented at the 2021 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Gastrointestinal Cancers Symposium by the lead investigator, Milind Javle, M.D., Professor of Gastrointestinal Medical Oncology at The University of Texas MD Anderson Cancer Center.

"While targeted treatments have extended survival for many types of cancer, people diagnosed with cholangiocarcinoma have previously been presented with extremely limited treatment options coupled with low statistical survival data," said Dr. Javle. "In this study, TRUSELTIQ showed promise as a targeted treatment option for patients with FGFR2-fusion-driven cholangiocarcinoma with a well-tolerated safety profile in line with previous observations in this patient population."

"The approval of TRUSELTIQ provides a new and exciting treatment option for patients with CCA harboring an FGFR2 fusion," said Stacie Lindsey, Chief Executive Officer of the Cholangiocarcinoma Foundation. "We appreciate the fact that there is a robust patient support program, ForgingBridges, to help patients access care and support them throughout their treatment journey."

Additional marketing applications for infigratinib are currently under review in Australia and Canada under Project Orbis, an initiative of the FDA’s Oncology Center of Excellence that allows for concurrent submission and review of oncology drugs among participating international regulatory agencies.

BridgeBio and Helsinn Group’s affiliate, Helsinn Therapeutics (U.S.), Inc., will be jointly responsible for commercialization activities in the U.S. and will share U.S. profits and losses on an equal basis. Helsinn Group will have exclusive commercialization rights on infigratinib outside of the U.S., excluding China, Hong Kong and Macau. BridgeBio will be eligible for tiered royalties as a percentage of adjusted net sales, and payments totaling up to approximately $2.45 billion USD in the aggregate. Helsinn Group will fund the majority of ongoing and future research and development related to infigratinib in oncology. BridgeBio and Helsinn Group entered into a global collaboration and licensing agreement in March 2021. BridgeBio previously entered a strategic collaboration with LianBio for development and commercialization of infigratinib in oncology indications in China, Hong Kong and Macau.

Paul Rittman, Chief Executive Officer of Helsinn Therapeutics, said, "Today’s FDA approval of TRUSELTIQ for patients with previously-treated locally advanced or metastatic CCA harboring an FGFR2 fusion or rearrangement provides a new therapy option for patients with a very low rate of survival. This new therapy has the potential to make a life changing impact on patients with few treatment options, and Helsinn Therapeutics looks forward to working with BridgeBio to make it widely accessible to health care providers and patients in the US."

ForgingBridges | TRUSELTIQ is a comprehensive patient support program designed specifically to provide education, access and affordability resources for patients during their TRUSELTIQ journey. For more information, visit: TRUSELTIQ.com/forgingbridges-overview.

Visit TRUSELTIQ.com for more information, including full Prescribing Information.

About TRUSELTIQ (infigratinib)
TRUSELTIQ (infigratinib) is an orally administered, ATP-competitive, tyrosine kinase inhibitor of FGFR, approved for the treatment of individuals with FGFR2 fusion-driven cholangiocarcinoma (bile duct cancer). TRUSELTIQ targets the fibroblast growth factor receptor (FGFR) protein, blocking downstream activity. In clinical studies, TRUSELTIQ demonstrated a clinically meaningful rate of tumor shrinkage (overall response rate) and duration of response. Visit TRUSELTIQ.com for more information. Infigratinib is not FDA approved for any other indication in the U.S. and is not approved for use by any other health authority. It is currently being evaluated in clinical studies for first-line cholangiocarcinoma and urothelial carcinoma (bladder cancer). For more information, visit QEDTx.com.

About Cholangiocarcinoma (CCA)
Cholangiocarcinoma, a cancer of the bile ducts of the liver, is a serious and often fatal disease which affects approximately 20,000 people in the United States and European Union each year. FGFR2 genetic aberrations are present in approximately 15% to 20% of people who have this disease. Currently, the five-year survival rate is only 9%.1 Advanced, unresectable CCA is a rare, aggressive malignancy with a poor prognosis.

Clinical Studies1
The efficacy of TRUSELTIQ was based on a single-arm Phase 2 study which included 108 patients with previously treated, unresectable locally advanced or metastatic cholangiocarcinoma with an FGFR2 fusion or rearrangement. Ninety-nine percent of patients had metastatic (Stage IV) disease at the time of study entry.

These 108 adult patients with advanced/metastatic CCA received infigratinib 125 mg orally for 21 days of each 28-day cycle until unacceptable toxicity or disease progression. All patients received prophylaxis with the oral phosphate binder sevelamer. TRUSELTIQ achieved a 23% objective response rate (ORR) and a median duration of response (DOR) of 5.0 months.

U.S. Indication for TRUSELTIQ
TRUSELTIQ is indicated for the treatment of adults with previously treated, unresectable locally advanced or metastatic cholangiocarcinoma with a fibroblast growth factor receptor 2 (FGFR2) fusion or other rearrangement as detected by an FDA-approved test.

Accelerated approval was granted based on overall response rate and duration of response. Continued approval for this indication may be contingent upon verification of clinical benefit in confirmatory trial(s).

U.S. Important Safety Information for TRUSELTIQ
Warnings and precautions

Ocular toxicity: Retinal pigment epithelial detachment (RPED), which may cause blurred vision, occurred in 11% of 351 patients treated with TRUSELTIQ, including patients with asymptomatic RPED, with a median onset of 26 days. Perform comprehensive ophthalmological exam including optical coherence tomography prior to initiating, at 1 month, at 3 months, and then every 3 months during treatment with TRUSELTIQ. Urgently evaluate patients for onset of visual symptoms and follow up every 3 weeks until resolved or TRUSELTIQ is discontinued. Withhold TRUSELTIQ as recommended. Dry eye occurred in 29% of 351 patients; treat with ocular demulcents as needed
Hyperphosphatemia and soft tissue mineralization: Hyperphosphatemia, which can lead to soft tissue mineralization, cutaneous calcinosis, non-uremic calciphylaxis, vascular calcification, and myocardial calcification, occurred in 82% of 351 patients treated with TRUSELTIQ, with a median time to onset of 8 days (range 1-349); 83% of 351 patients treated with TRUSELTIQ received phosphate binders. Monitor for hyperphosphatemia throughout treatment. Initiate phosphate-lowering therapy for serum phosphate >5.5 mg/dL; withhold TRUSELTIQ and initiate phosphate-lowering therapy for serum phosphate >7.5 mg/dL; withhold, reduce the dose, or permanently discontinue TRUSELTIQ based on duration and severity of hyperphosphatemia
Embryo-fetal toxicity: TRUSELTIQ can cause fetal harm. Advise pregnant women of the potential risk to the fetus; advise females of reproductive potential and men who are partnered with women of reproductive potential to use effective contraception during treatment with TRUSELTIQ and for 1 month after the final dose
Adverse reactions

Most common adverse reactions (incidence ≥20%, all grades): nail toxicity, stomatitis, dry eye, fatigue, alopecia, palmar-plantar erythrodysesthesia syndrome, arthralgia, dysgeusia, constipation, abdominal pain, dry mouth, eyelash changes, diarrhea, dry skin, decreased appetite, blurred vision, and vomiting
Most common laboratory abnormalities (incidence ≥20%, all grades): increased creatinine, increased phosphate, decreased phosphate, increased alkaline phosphatase, decreased hemoglobin, increased alanine aminotransferase, increased lipase, increased calcium, decreased lymphocytes, decreased sodium, increased triglycerides, increased aspartate aminotransferase (AST), increased urate, decreased platelets, decreased leukocytes, decreased albumin, increased bilirubin, and decreased potassium
Drug interactions

CYP3A inhibitors: Avoid use with strong and moderate CYP3A inhibitors
CYP3A inducers: Avoid use with strong and moderate CYP3A inducers
Gastric acid–reducing agents: Avoid coadministration with proton pump inhibitors, histamine-2 receptor antagonists (H2RA), and locally acting antacids. If coadministration of H2RA or locally acting antacids cannot be avoided, separate TRUSELTIQ administration
H2RA: Take TRUSELTIQ 2 hours before or 10 hours after
Locally-acting antacid: Take TRUSELTIQ 2 hours before or 2 hours after
Dosage and administration

Prior to initiating TRUSELTIQ: Confirm FGFR2 fusion or rearrangement; perform comprehensive ophthalmic exam including OCT; confirm negative pregnancy test in females of reproductive potential
Starting dose: Take TRUSELTIQ orally once daily on Days 1-21 of 28-day cycles; continue treatment until disease progression or unacceptable toxicity. Take TRUSELTIQ on an empty stomach with a glass of water at least 1 hour before or 2 hours after food
No renal or hepatic impairment
125 mg (one 100 mg capsule and one 25 mg capsule)
Mild and moderate renal impairment (creatinine clearance 30-89 mL/min)
100 mg (one 100 mg capsule)
Mild hepatic impairment (total bilirubin >upper limit of normal [ULN] to 1.5 x ULN or AST > ULN)
100 mg (one 100 mg capsule)
Moderate hepatic impairment (total bilirubin >1.5 to 3 x ULN with any AST)
75 mg (three 25 mg capsules)
Dose modification: Consult the TRUSELTIQ full Prescribing Information for dose modifications and monitoring recommendations for RPED, hyperphosphatemia, and other Grades 3-4 adverse reactions

On May 28, 2021 Amgen (NASDAQ: AMGN) reported that the U.S. Food and Drug Administration (FDA) has approved LUMAKRAS (sotorasib) for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA-approved test, who have received at least one prior systemic therapy (Press release, Amgen, MAY 28, 2021, View Source [SID1234583263]). LUMAKRAS has received accelerated approval based on overall response rate (ORR) and duration of response (DoR). Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).

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To view the multimedia assets associated with this release, please click: View Source

"The FDA approval of LUMAKRAS is a breakthrough moment for patients with KRAS G12C-mutated non-small cell lung cancer because there is now a targeted therapy for this common, but previously elusive, mutation," said David M. Reese, M.D., executive vice president of Research and Development at Amgen. "KRAS has challenged cancer researchers for more than 40 years with many deeming it as ‘undruggable.’ The LUMAKRAS development program was a race against cancer for Amgen’s scientists and clinical trial investigators who together have now successfully delivered this new medicine to patients in less than three years—from first patient dosed to U.S. regulatory approval."

The FDA approval of LUMAKRAS is based on results from a subset of patients in CodeBreaK 100, the largest clinical trial conducted to date exclusively for patients with the KRAS G12C mutation. The trial demonstrated favorable efficacy and tolerability in 124 patients with KRAS G12C mutation-positive NSCLC who had disease progression after receiving an immunotherapy and/or chemotherapy. In the trial, 960 mg of LUMAKRAS administered orally once-daily demonstrated an ORR (a proportion of patients with ≥ 30% decrease in tumor) of 36% (95% CI: 28-45) with 81% (95% CI: 73-87) of patients achieving disease control (percentage of patients who have achieved complete response, partial response and stable disease for more than three months). The median DoR was 10 months. The most common adverse reactions (≥ 20%) were diarrhea, musculoskeletal pain, nausea, fatigue, hepatotoxicity and cough. Adverse reactions resulting in permanent discontinuation of LUMAKRAS occurred in 9% of patients.

"Sotorasib represents a major advancement in oncology and changes the treatment paradigm for patients with KRAS G12C-mutated non-small cell lung cancer," said Bob T. Li, M.D., Ph.D., MPH, principal investigator at Memorial Sloan Kettering Cancer Center. "Patients with non-small cell lung cancer who have progressed beyond first-line treatment face a poor prognosis and have limited treatment options available to them. Sotorasib delivers a new option for these patients, and it is the first KRAS-targeted therapy to be approved after nearly four decades of research."

NSCLC accounts for approximately 84% of the 2.2 million new lung cancer diagnoses each year worldwide, including approximately 236,000 new cases in the U.S.2,3 KRAS G12C is one of the most prevalent driver mutations in NSCLC, with about 13% of patients with non-squamous NSCLC in the U.S. having the KRAS G12C mutation.1

Amgen’s Commitment to Comprehensive Biomarker Testing and Patient Support
About half of all patients with NSCLC harbor a targetable driver mutation, yet despite the integral role that biomarkers play in identifying patients who may benefit from targeted therapies, many patients are not tested.4,5

Amgen has partnered with two companies—Guardant Health and QIAGEN—to develop blood- and tissue-based companion diagnostics (CDx), respectively, for LUMAKRAS. With the addition of these tests, patients and clinicians will have more options and flexibility for conducting KRAS G12C biomarker testing.

"Biomarker testing for patients with non-small cell lung cancer is critical because it informs a patient’s treatment path with a personalized and tailored approach. The only way to identify the KRAS G12C mutation is to test for it, so I urge patients to ask their care teams about comprehensive biomarker testing. It is important that patients and their healthcare providers know that KRAS G12C is now an actionable mutation," said Andrea Ferris, president and CEO of LUNGevity. "Today’s FDA approval of a therapy targeted for KRAS G12C, one of the most prevalent biomarkers in non-small cell lung cancer, brings hope to the many patients who carry this mutation and is a significant moment for the lung cancer community who need more innovative treatment options."

Amgen is committed to supporting patients with NSCLC and to helping appropriate patients with affordable access to LUMAKRAS. Patients, caregivers and physicians who need support, tools or resources can contact Amgen Assist360(1-888-4ASSIST). Amgen also provides patient assistance for its medicines marketed in the U.S. in a variety of ways, including free medicines through the Amgen Safety Net Foundation for qualifying individuals with no or limited drug coverage.

Amgen to Webcast Investor Call on LUMAKRAS FDA Approval
Amgen will host a webcast call for the investment community on Tuesday, June 1, 2021 at 5 a.m. PT / 8 a.m. ET. David M. Reese, M.D., executive vice president of Research and Development and Murdo Gordon, executive vice president of Global Commercial Operations at Amgen will participate to discuss the recent FDA approval of LUMAKRAS.

Live audio of the investor call will be simultaneously broadcast over the Internet and will be available to members of the news media, investors and the general public.

The webcast, as with other selected presentations regarding developments in Amgen’s business given by management at certain investor and medical conferences, can be found on Amgen’s website, www.amgen.com, under Investors. Information regarding presentation times, webcast availability and webcast links are noted on Amgen’s Investor Relations Events Calendar. The webcast will be archived and available for replay for at least 90 days after the event.

About LUMAKRAS (sotorasib)
Amgen has taken on one of the toughest challenges of the last 40 years in cancer research by developing LUMAKRAS, a KRASG12C inhibitor.6 LUMAKRAS was the first KRASG12C inhibitor to enter the clinic and is being studied in the largest clinical program exploring 11 combinations with global investigator sites spanning five continents.

LUMAKRAS has demonstrated a positive benefit-risk profile with rapid, deep and durable anticancer activity in patients with locally advanced and metastatic non-small cell lung cancer (NSCLC) harboring the KRAS G12C mutation with a once daily oral formulation. As part of the evaluation for this accelerated approval, FDA is requiring a post-marketing trial to investigate whether a lower dose will have a similar clinical effect.

LUMAKRAS is also being studied in multiple other solid tumors.6

In the U.S., LUMAKRAS was reviewed by the FDA under its Real-Time Oncology Review (RTOR), a pilot program that aims to explore a more efficient review process that ensures safe and effective treatments are made available to patients as early as possible. Amgen submitted a Marketing Authorization Application (MAA) in the EU in December 2020 and New Drug Applications in Japan (J-NDA) and Switzerland in April 2021. Additionally, Amgen submitted MAAs for sotorasib in Australia, Brazil, Canada and the United Kingdom in January 2021 to participate in the FDA’s Project Orbis initiative. Sotorasib was granted Breakthrough Therapy Designation in the U.S. and China.

LUMAKRAS (sotorasib) U.S. Indication
LUMAKRAS is indicated for the treatment of adult patients with KRAS G12C-mutated locally advanced or metastatic non-small cell lung cancer (NSCLC), as determined by an FDA-approved test, who have received at least one prior systemic therapy.

This indication is approved under accelerated approval based on overall response rate (ORR) and duration of response (DOR). Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).

LUMAKRAS (sotorasib) Important Safety Information

Hepatotoxicity

LUMAKRAS can cause hepatotoxicity, which may lead to drug-induced liver injury and hepatitis.
Among 357 patients who received LUMAKRAS in CodeBreaK 100, hepatotoxicity occurred in 1.7% (all grades) and 1.4% (Grade 3). A total of 18% of patients who received LUMAKRAS had increased alanine aminotransferase (ALT)/increased aspartate aminotransferase (AST); 6% were Grade 3 and 0.6% were Grade 4. In addition to dose interruption or reduction, 5% of patients received corticosteroids for the treatment of hepatotoxicity.
Monitor liver function tests (ALT, AST, and total bilirubin) prior to the start of LUMAKRAS, every 3 weeks for the first 3 months of treatment, then once a month or as clinically indicated, with more frequent testing in patients who develop transaminase and/or bilirubin elevations.
Withhold, dose reduce or permanently discontinue LUMAKRAS based on severity of adverse reaction.
Interstitial Lung Disease (ILD)/Pneumonitis

LUMAKRAS can cause ILD/pneumonitis that can be fatal. Among 357 patients who received LUMAKRAS in CodeBreaK 100 ILD/pneumonitis occurred in 0.8% of patients, all cases were Grade 3 or 4 at onset, and 1 case was fatal. LUMAKRAS was discontinued due to ILD/pneumonitis in 0.6% of patients.
Monitor patients for new or worsening pulmonary symptoms indicative of ILD/pneumonitis (e.g., dyspnea, cough, fever). Immediately withhold LUMAKRAS in patients with suspected ILD/pneumonitis and permanently discontinue LUMAKRAS if no other potential causes of ILD/pneumonitis are identified.
Most Common Adverse Reactions

The most common adverse reactions ≥ 20% were diarrhea, musculoskeletal pain, nausea, fatigue, hepatotoxicity, and cough.
Drug Interactions

Advise patients to inform their healthcare provider of all concomitant medications, including prescription medicines, over-the-counter drugs, vitamins, dietary and herbal products.
Inform patients to avoid proton pump inhibitors and H2 receptor antagonists while taking LUMAKRAS.
If coadministration with an acid-reducing agent cannot be avoided, inform patients to take LUMAKRAS 4 hours before or 10 hours after a locally acting antacid.
Please see LUMAKRAS full Prescribing Information.

About Non-Small Cell Lung Cancer and the KRAS G12C Mutation
Lung cancer is the leading cause of cancer-related deaths worldwide, and it accounts for more deaths worldwide than colon cancer, breast cancer and prostate cancer combined.3 Overall survival rates for NSCLC are improving, but remain poor for patients with advanced disease and 5-year survival is only 7% for those with metastatic disease.7

KRAS G12C is the most common KRAS mutation in NSCLC.8 In the U.S., about 13% of patients with non-squamous NSCLC harbor the KRAS G12C mutation.1 Unmet medical need remains high and treatment options are limited for NSCLC patients with the KRAS G12C mutation whose first-line treatment has failed to work or has stopped working. The outcomes with current therapies are suboptimal with a median progression-free survival of approximately 4 months following second-line treatment of KRAS G12C-mutated NSCLC.9

About CodeBreaK
The CodeBreaK clinical development program for Amgen’s drug sotorasib is designed to treat patients with an advanced solid tumor with the KRAS G12C mutation and address the longstanding unmet medical need for these cancers. As the most advanced KRAS G12C clinical development program, CodeBreaK has enrolled more than 800 patients across 13 tumor types since its inception.

CodeBreaK 100, the Phase 1 and 2, first-in-human, open-label multicenter study, enrolled patients with KRAS G12C-mutant solid tumors. Eligible patients must have received a prior line of systemic anticancer therapy, consistent with their tumor type and stage of disease. The primary endpoint for the Phase 2 study was centrally assessed objective response rate. The Phase 2 trial in NSCLC enrolled 126 patients, 124 of whom had centrally evaluable lesions by RECIST at baseline. The Phase 2 trial in colorectal cancer (CRC) is fully enrolled and topline results are expected later in 2021.

A global Phase 3 randomized active-controlled study comparing sotorasib to docetaxel in patients with KRAS G12C-mutated NSCLC (CodeBreaK 200) has completed enrollment. Amgen also has several Phase 1b studies investigating sotorasib monotherapy and sotorasib combination therapy across various advanced solid tumors (CodeBreaK 101) open for enrollment.

About Amgen Oncology
At Amgen Oncology, our mission to serve patients drives all that we do. That’s why we’re relentlessly focused on accelerating the delivery of medicines that have the potential to empower all angles of care and transform lives of people with cancer.

For the last four decades, we have been dedicated to discovering the firsts that matter in oncology and to finding ways to reduce the burden of cancer. Building on our heritage, Amgen continues to advance the largest pipeline in the Company’s history, moving with great speed to advance those innovations for the patients who need them.

At Amgen, we’re advancing oncology at the speed of life.