INDICATION AND LIMITATIONS OF USE

Vectibix® is indicated for the treatment of adult patients with wild-type RAS (defined as wild-type in both KRAS and NRAS as determined by an FDA-approved test) metastatic colorectal cancer (mCRC): Read More

Vectibix® is indicated for the treatment of adult patients with wild-type RAS (defined as wild-type in both KRAS and NRAS as determined by an FDA-approved test) metastatic colorectal cancer (mCRC): Read More

Prescribing Information Indication Important Safety Information Patient Site
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Your choices matter: Explore the appropriate 1L treatment of mCRC through biomarker status and primary tumor location1

TUMOR FACTORS THAT CAN GUIDE TREATMENT DECISIONS IN PATIENTS NEWLY DIAGNOSED WITH mCRC:2,3

Actionable-biomarkers
molecular-biomarkers-sm
Primary-tumor-location
Primary-tumor-location-mb

CLINICAL GUIDELINES RECOMMEND TARGETED TREATMENT OF mCRC BASED ON BIOMARKER STATUS AND SIDEDNESS1,4

SEE THE PATHWAY

GUIDELINE-RECOMMENDED TREATMENT

Anti-EGFR plus chemotherapy is part of certain 1L targeted treatment recommendations for left-sided mCRC from the National Comprehensive Cancer Network® (NCCN®) and ASCO4,5

NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®)

NCCN Category 2A panitumumab is a recommended option for 1L in combination with FOLFOX for non-MSI-H, KRAS/NRAS/BRAF WT* and left-sided mCRC.4

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.

*Patients with BRAF mutations other than V600E may be candidates for anti-EGFR therapy.4

ASCO GUIDELINES

Clinical guidelines recommend targeted treatment of mCRC based on biomarker status and sidedness1,5
SEE THE PATHWAY

GUIDELINE-RECOMMENDED TREATMENT IMPROVES OUTCOMES IN mCRC

In a real-world study, improved median overall survival was observed with 1L anti-EGFR therapy in patients with WT RAS and WT BRAF, left-sided mCRC.6

Targeted treatment reshapes outcomes in mCRC
Targeted treatment reshapes outcomes in mCRC

1L = first line; 5-FU = 5-fluorouracil; EGFR = epidermal growth factor receptor; ICD = International Classification of Diseases; mCRC = metastatic colorectal cancer; VEGF = vascular endothelial growth factor; WT = wild type.

Based on a retrospective review of patient data from the nationwide Flatiron Health database of de-identified electronic health records covering approximately 800 sites of care at ~280 US cancer clinics. Included patients were diagnosed with mCRC between January 2013 and December 2018 and received a standard first-line chemotherapy doublet defined as 5-FU/oxaliplatin (FOLFOX), capecitabine/oxaliplatin (CAPEOX), or 5-FU/irinotecan (FOLFIRI). Within this group, only patients who were documented as having RAS/RAF WT mCRC with a left-sided primary tumor (LSPT) as determined by ICD coding were included in the final analysis. LSPT defined as those located in the splenic flexure, descending, sigmoid, and rectum. Targeted therapy included anti-VEGF (bevacizumab) and anti-EGFR agents (cetuximab or panitumumab), which was considered part of first-line therapy if it was added within 2 months of the first administered dose of chemotherapy. Of 20,333 patients with mCRC included in the EHR-derived dataset, 9,753 received a standard chemotherapy doublet with or without targeted therapy. A tumor sidedness–specific ICD code was entered for 2,449 patients, with 1,607 documented as having an LSPT. Within the cohort, 456 patients received first-line chemotherapy alone, 965 received chemotherapy plus bevacizumab, and 186 received chemotherapy plus an anti-EGFR agent. When stratified by first-line therapy received, groups were balanced with regard to race, gender, performance status, disease presentation (recurrent vs de novo metastatic disease), and documented location of primary tumor.6

NEARLY 2 OUT OF 3* mCRC PATIENTS MAY BE CLINICALLY ELIGIBLE FOR BIOMARKER-DRIVEN FDA-APPROVED THERAPY

PREVALENCE OF MUTATIONS IN MOLECULAR BIOMARKERS IN mCRC3,†

Prevalence of actionable biomarkers in mCRC
Prevalence of actionable biomarkers in mCRC

*44% RAS WT + 9% BRAF + 5% MSI + 5% HER2-amplified = 63%.

†Percentages are approximations. Overlapping aberrations may be observed in some tumors.

‡BRAF V600E mutation.3

BRAF = v‑raf murine sarcoma viral oncogene homolog B1; HER2 = human epidermal growth factor receptor 2; KRAS = Kristen rat sarcoma viral oncogene homolog; mCRC = metastatic colorectal cancer; MSI-H = microsatellite instability-high; MSI-H = microsatellite instability-low; MSS = microsatellite stable; MT = mutant type; NRAS = neuroblastoma rat sarcoma viral oncogene homolog; NTRK = neurotrophic tyrosine receptor kinase; RAS = rat sarcoma viral oncogene homolog; WT = wild‑type.

clinical practice guidelines recommend testing patients with mCRC for clinically relevant biomarkers4,7,8

Major international clinical practice guidelines recommend testing patients with mCRC for clinically relevant biomarkers
Major international clinical practice guidelines recommend testing patients with mCRC for clinically relevant biomarkers

ASCO = American Society of Clinical Oncology; ESMO = European Society of Medical Oncology; MMR = mismatch repair; MSI = microsatellite instability.

TESTING ENABLES TARGETED TREATMENT

Biomarker knowledge supports precise patient identification for 1L anti-EGFR targeted therapy3,8

RATES OF BIOMARKER TESTING IN mCRC ARE TRENDING UPWARDS, BUT STILL FALL SHORT OF GUIDELINE RECOMMENDATIONS9

Group of people at ideal state of 100% of patients with mCRC tested for all relevant biomarkers
Group of people at ideal state of 100% of patients with mCRC tested for all relevant biomarkers

arrow Guideline Recommended: 100% of patients with mCRC tested for all relevant biomarkers9

BIOMARKER TESTING RATES ACROSS VARIED SITES OF CARE9

N = 20,333

Group of people at ideal state of 100% of patients with mCRC tested for all relevant biomarkers
Current state: 66.6% of patients with mCRC are tested for either KRAS, NRAS, or BRAF9
Current state: 30.5% of patients with mCRC are tested for all 3 biomarkers (KRAS, NRAS, and BRAF)9
Current state: ~55% of patients with mCRC are tested for MSI/MMR9

Based on a retrospective cohort study of patient data from the nationwide Flatiron Health database of de-identified electronic health records covering approximately 800 sites of care at ~280 US cancer clinics. All patients were aged 18 or older with de novo metastatic or a metastatic recurrence diagnosed with mCRC between January 1, 2013 and December 31, 2018. A patient was counted as “tested” if they underwent testing within 6 months of their diagnosis. A total of 20,333 patients were included in the analysis. Most patients (93.1%) were treated at community centers and 6.9% were treated at academic centers.9

MORE COMPREHENSIVE BIOMARKER TESTING HAS THE POTENTIAL TO OPTIMIZE TREATMENT & IMPROVE OUTCOMES

Select an appropriate biomarker test4,7,11,12

Select an approriate biomarker test with biopsy type, turnaround time, and CRC biomarker(s)
Select an approriate biomarker test with biopsy type, turnaround time, and CRC biomarker(s)

*Turnaround time is the time from which the sample arrives at the testing laboratory to when the oncologist/ordering physician receives the test results. ASCP/CAP/AMP/ASCO guidelines recommend a 10-working day turnaround time for the majority of tests.

1L = first line; CAP = College of American Pathologists; CRC = colorectal cancer; AMP = Association for Molecular Pathology: ASCO = American Society of Clinical Oncology: ASCP = American Society for Clinical Pathology; EGFR = epidermal growth factor receptor; HER2 = human epidermal growth factor receptor 2; mCRC = metastatic colorectal cancer; MMR = mismatch repair deficient; MSI = microsatellite instability; PCR = polymerase chain reaction; WT = wild type.

NEXT, FACTOR IN TUMOR SIDEDNESS

Identifying patients with WT RAS, WT BRAF, non-MSI-H, left-sided mCRC represents a paradigm shift to refine 1L targeted treatment selection2

TWO OUT OF THREE PATIENTS WITH mCRC HAVE LEFT-SIDED TUMORS13

Diagram of left-sided tumors for mCRC patients
Diagram of left-sided tumors for mCRC patients

ANTI-EGFR THERAPY FOR 1L LEFT-SIDED WT RASRAS* mCRC6

ASCO GUIDELINES: SYSTEMIC THERAPY FOR mCRC ALGORITHM5

Systemic therapy for metastatic colorectal cancer (mCRC) Algorithm
Systemic therapy for metastatic colorectal cancer (mCRC) Algorithm

For full treatment guidelines see Morris VK, et al. J Clin Oncol. 2023;41:678-700.

*Defined as wild type in both KRAS and NRAS.13

†Decisions regarding treatment options and sequencing for all patients with mCRC should be made within the context of an MDT.

‡Doublet CT should be offered, or triplet CT may be offered. Shared decision-making is recommended, including a discussion of the potential for benefit and risk of harm; while survival and recurrence outcomes are improved, grade 3 or greater adverse events are more frequent with triplet CT compared to doublet CT.

§Anti-EGFR therapy is not recommended for patients with RAS-mutant mCRC.

**Anti-EGFR therapy is not recommended as a lone biologic agent for treatment-naïve patients with BRAF V600E-mutant mCRC.

††Although anti-EGFR therapy is preferred, anti-VEGF therapy remains an active treatment option for patients with left-sided treatment-naïve RAS wild-type mCRC.

This algorithm is derived from recommendations in Treatment of Metastatic Colorectal Cancer: ASCO Guideline. This is a tool based on an ASCO Guideline and is not intended to substitute for the independent professional judgment of the treating physician. Practice guidelines do not account for individual variation among patients. This tool does not purport to suggest any particular course of medical treatment. Use of the guideline and this tool are voluntary.

ASCO = American Society of Clinical Oncology; CT = chemotherapy; dMMR = deficient mismatch repair; doublet CT = FOLFOX, CAPOX, or FOLFIRI; EGFR = epidermal growth factor receptor; mCRC = metastatic colorectal cancer; MDT = multidisciplinary team; MSI = microsatellite instability; triplet CT = FOLFOXIRI; VEGF = vascular endothelial growth factor.

PARADIGM reinforces the value of:

  • Conducting early biomarker testing to determine a patient’s RAS status
  • Including tumor sidedness as a criterion for the selection of biologic therapies
  • Prescribing Vectibix® + FOLFOX as 1L therapy in newly diagnosed patients with WT RAS* and left-sided mCRC

LEARN HOW VECTIBIX® CLINICAL DATA HELPED EVOLVE BIOMARKER-BASED DECISIONS FOR PATIENTS WITH mCRC

Vectibix® Podcast

VECTIBIX® PODCAST: BIOMARKER ANALYSIS FOR THE TREATMENT OF NEWLY DIAGNOSED mCRC

With Dr. Philip Philip and Dr. Kurt Tauer

Biomarker Analysis for the Treatment of Newly Diagnosed …

Drs. Philip and Tauer are paid consultants for Amgen.

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REVIEW CLINICAL DATA

IMPORTANT SAFETY INFORMATION

BOXED WARNING:
DERMATOLOGIC TOXICITY

Dermatologic Toxicity: Dermatologic toxicities occurred in 90% of patients and were severe (NCI-CTC Grade 3 and higher) in 15% of patients receiving Vectibix® monotherapy

  • Vectibix® can cause dermatologic toxicity, which may be severe. Clinical manifestations included, but were not limited to, acneiform dermatitis, pruritus, erythema, rash, skin exfoliation, paronychia, dry skin, and skin fissures.
  • Among 229 patients who received Vectibix® as monotherapy, dermatologic toxicity occurred in 90% including Grade 3 (15%). Among 585 patients who received Vectibix® in combination with FOLFOX, dermatologic toxicity occurred in 96% including Grade 4 (1%) and Grade 3 (32%). In 126 patients receiving Vectibix® in combination with sotorasib across clinical studies, dermatologic toxicities occurred in 94%, including Grade 3 (16%) of patients.
  • Monitor patients who develop dermatologic or soft tissue toxicities while receiving Vectibix® for the development of inflammatory or infectious sequelae. Life-threatening and fatal infectious complications including necrotizing fasciitis, abscesses, and sepsis have been observed in patients treated with Vectibix®. Life-threatening and fatal bullous mucocutaneous disease with blisters, erosions, and skin sloughing has also been observed in patients treated with Vectibix®. It could not be determined whether these mucocutaneous adverse reactions were directly related to EGFR inhibition or to idiosyncratic immune- related effects (eg, Stevens Johnson syndrome or toxic epidermal necrolysis). Withhold or discontinue Vectibix® for dermatologic or soft tissue toxicity associated with severe or life-threatening inflammatory or infectious complications. Dose modifications for Vectibix® concerning dermatologic toxicity are provided.
  • Vectibix® monotherapy or in combination with oxaliplatin-based chemotherapy is not indicated for the treatment of patients with colorectal cancer that harbor somatic RAS mutations in exon 2 (codons 12 and 13), exon 3 (codons 59 and 61), and exon 4 (codons 117 and 146) of either KRAS or NRAS and hereafter is referred to as “RAS.”
  • Retrospective subset analyses across several randomized clinical trials were conducted to investigate the role of RAS mutations on the clinical effects of anti-EGFR-directed monoclonal antibodies (panitumumab or cetuximab). Anti-EGFR antibodies in patients with tumors containing RAS mutations resulted in exposing those patients to anti-EGFR related adverse reactions without clinical benefit from these agents. Additionally, in Study 20050203, 272 patients with RAS-mutant mCRC tumors received Vectibix® in combination with FOLFOX and 276 patients received FOLFOX alone. In an exploratory subgroup analysis, OS was shorter (HR = 1.21, 95% CI: 1.01-1.45) in patients with RAS-mutant mCRC who received Vectibix® and FOLFOX versus FOLFOX alone.
  • Vectibix® can cause progressively decreasing serum magnesium levels leading to severe (Grade 3 or 4) hypomagnesemia. Among 229 patients who received Vectibix® as monotherapy, hypomagnesemia occurred in 38% including Grade 4 (1.3%) and Grade 3 (2.6%). Among 585 patients who received Vectibix® in combination with FOLFOX, hypomagnesemia occurred in 51% including Grade 4 (5%) and Grade 3 (6%). In 126 patients receiving Vectibix® in combination with sotorasib across clinical studies, decreased magnesium occurred in 69%, including Grade 4 (2.4%) and Grade 3 (14%).
  • Monitor patients for hypomagnesemia and hypocalcemia prior to initiating Vectibix® treatment, periodically during Vectibix® treatment, and for up to 8 weeks after the completion of treatment. Other electrolyte disturbances, including hypokalemia, have also been observed. Replete magnesium and other electrolytes as appropriate.
  • In Study 20020408, 4% of patients experienced infusion reactions and 1% of patients experienced severe infusion reactions (NCI-CTC Grade 3-4). Infusion reactions, manifesting as fever, chills, dyspnea, bronchospasm, and hypotension, can occur following Vectibix® administration. Fatal infusion reactions occurred in postmarketing experience. Terminate the infusion for severe infusion reactions.
  • Severe diarrhea and dehydration, leading to acute renal failure and other complications, have been observed in patients treated with Vectibix®. Among 229 patients who received Vectibix® as monotherapy, acute renal failure occurred in 2% including Grades 3 or 4 (2%). Among 585 patients who received Vectibix® in combination with FOLFOX, acute renal failure occurred in 2% including Grade 3 or 4 (2%). In 126 patients receiving Vectibix® in combination with sotorasib across clinical studies, acute renal failure occurred in 3.2%, including Grade 3 (0.8%). Monitor patients for diarrhea and dehydration, provide supportive care (including anti-emetic or anti-diarrheal therapy) as needed, and withhold Vectibix® if necessary.
  • Fatal and nonfatal cases of interstitial lung disease (ILD) (1%) and pulmonary fibrosis have been observed in patients treated with Vectibix®. Pulmonary fibrosis occurred in less than 1% (2/1467) of patients enrolled in clinical studies of Vectibix®. Grade 1 ILD/pneumonitis occurred in 0.8% (1/126) of patients enrolled in clinical studies of Vectibix® in combination with sotorasib. In the event of acute onset or worsening of pulmonary symptoms interrupt Vectibix® therapy. Discontinue Vectibix® therapy if ILD is confirmed.
  • In patients with a history of interstitial pneumonitis or pulmonary fibrosis, or evidence of interstitial pneumonitis or pulmonary fibrosis, the benefits of therapy with Vectibix® versus the risk of pulmonary complications must be carefully considered.
  • Exposure to sunlight can exacerbate dermatologic toxicity. Advise patients to wear sunscreen and hats and limit sun exposure while receiving Vectibix®.
  • Serious cases of keratitis, ulcerative keratitis, and corneal perforation have occurred with Vectibix® use. Among 585 patients who received Vectibix® in combination with FOLFOX, keratitis occurred in 0.3%. In 126 patients receiving Vectibix® in combination with sotorasib across clinical studies, keratitis occurred in 1.6%, ulcerative keratitis occurred in 0.8%, and vernal keratoconjunctivitis in 0.8% (all were Grade 1-2). Monitor for evidence of keratitis, ulcerative keratitis, or corneal perforation. Interrupt or discontinue Vectibix® therapy for acute or worsening keratitis, ulcerative keratitis, or corneal perforation.
  • In an interim analysis of an open-label, multicenter, randomized clinical trial in the first-line setting in patients with mCRC, the addition of Vectibix® to the combination of bevacizumab and chemotherapy resulted in decreased OS and increased incidence of NCI-CTC Grade 3-5 (87% vs 72%) adverse reactions. NCI-CTC Grade 3-4 adverse reactions occurring at a higher rate in Vectibix®-treated patients included rash/acneiform dermatitis (26% vs 1%), diarrhea (23% vs 12%), dehydration (16% vs 5%), primarily occurring in patients with diarrhea, hypokalemia (10% vs 4%), stomatitis/mucositis (4% vs <1%), and hypomagnesemia (4% vs 0). NCI-CTC Grade 3-5 pulmonary embolism occurred at a higher rate in Vectibix®-treated patients (7% vs 3%) and included fatal events in three (< 1%) Vectibix® -treated patients.
  • As a result of the toxicities experienced, patients randomized to Vectibix®, bevacizumab, and chemotherapy received a lower mean relative dose intensity of each chemotherapeutic agent (oxaliplatin, irinotecan, bolus 5-FU, and/or infusional 5-FU) over the first 24 weeks on study compared with those randomized to bevacizumab and chemotherapy.
  • Based on data from animal studies and its mechanism of action, Vectibix® can cause fetal harm when administered to a pregnant woman. When given during organogenesis, panitumumab administration resulted in embryolethality in cynomolgus monkeys at exposures approximately 1.25 to 5 times the recommended human dose. Advise pregnant women and females of reproductive potential of the potential risk to the fetus. Advise females of reproductive potential to use effective contraception during treatment, and for at least 2 months after the last dose of Vectibix®.
  • In monotherapy, the most commonly reported adverse reactions (≥ 20%) in patients with Vectibix® were skin rash with variable presentations, paronychia, fatigue, nausea, and diarrhea.
  • The most commonly reported adverse reactions (≥ 20%) with Vectibix® + FOLFOX were diarrhea, stomatitis, mucosal inflammation, asthenia, paronychia, anorexia, hypomagnesemia, hypokalemia, rash, acneiform dermatitis, pruritus, and dry skin. Serious adverse reactions (≥ 2% difference between treatment arms) were diarrhea and dehydration.

INDICATION

Vectibix® is indicated for the treatment of adult patients with wild-type RAS (defined as wild-type in both KRAS and NRAS as determined by an FDA-approved test) metastatic colorectal cancer (mCRC):

  • As first-line therapy in combination with FOLFOX.
  • As monotherapy following disease progression after prior treatment with fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy.

LIMITATIONS OF USE

Vectibix® is not indicated for the treatment of patients with RAS-mutant mCRC unless used in combination with sotorasib in KRAS G12C-mutated mCRC. Vectibix® is not indicated for the treatment of patients with mCRC for whom RAS mutation status is unknown.

For information about the use of Vectibix® in combination with sotorasib, see Vectibix® Prescribing Information.

Please see Vectibix® full Prescribing Information, including Boxed WARNING.

IMPORTANT SAFETY INFORMATION FOR LUMAKRAS®

  • LUMAKRAS can cause hepatotoxicity and increased ALT or AST which may lead to drug-induced liver injury and hepatitis.
  • In the pooled safety population of NSCLC patients who received single agent LUMAKRAS 960 mg hepatotoxicity occurred in 27% of patients, of which 16% were Grade ≥ 3. Among patients with hepatotoxicity who required dosage modifications, 64% required treatment with corticosteroids.
  • In this pooled safety population of NSCLC patients who received single agent LUMAKRAS 960 mg, 17% of patients who received LUMAKRAS had increased alanine aminotransferase (ALT)/increased aspartate aminotransferase (AST); of which 9% were Grade ≥ 3. The median time to first onset of increased ALT/AST was 6.3 weeks (range: 0.4 to 42). Increased ALT/AST leading to dose interruption or reduction occurred in 9% of patients treated with LUMAKRAS. LUMAKRAS was permanently discontinued due to increased ALT/AST in 2.7% of patients. Drug-induced liver injury occurred in 1.6% (all grades) including 1.3% (Grade ≥ 3).
  • In this pooled safety population of NSCLC patients who received single agent LUMAKRAS 960 mg, a total of 40% patients with recent (≤ 3 months) immunotherapy prior to starting LUMAKRAS had an event of hepatotoxicity. An event of hepatotoxicity was observed in 18% of patients who started LUMAKRAS more than 3 months after last dose of immunotherapy and in 17% of those who never received immunotherapy. Regardless of time from prior immunotherapy, 94% of hepatotoxicity events improved or resolved with dosage modification of LUMAKRAS, with or without corticosteroid treatment.
  • Monitor liver function tests (ALT, AST, alkaline phosphatase 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, reduce the dose or permanently discontinue LUMAKRAS based on severity of the adverse reaction. Consider administering systemic corticosteroids for the management of hepatotoxicity.

Interstitial Lung Disease (ILD)/Pneumonitis

  • LUMAKRAS can cause ILD/pneumonitis that can be fatal.
  • In the pooled safety population of NSCLC patients who received single agent LUMAKRAS 960 mg ILD/pneumonitis occurred in 2.2% of patients, of which 1.1% were Grade ≥ 3, and 1 case was fatal. The median time to first onset for ILD/pneumonitis was 8.6 weeks (range: 2.1 to 36.7 weeks). LUMAKRAS was permanently discontinued due to ILD/pneumonitis in 1.3% of LUMAKRAS-treated 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.

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).

Please see accompanying LUMAKRAS® full Prescribing Information.

IMPORTANT SAFETY INFORMATION

BOXED WARNING:
DERMATOLOGIC TOXICITY

Dermatologic Toxicity: Dermatologic toxicities occurred in 90% of patients and were severe (NCI-CTC Grade 3 and higher) in 15% of patients receiving Vectibix® monotherapy

References 1. Morris VK, Kennedy EB, Baxter NN, et al. J Clin Oncol. 2023;41:678-700. 2. Doleschal B, Petzer A, Rumpold H. Front Oncol. 2022;12:1048166. 3. Cohen R, Pudlarz T, Delattre JF, Colle R, André T. Cancers (Basel). 2020;12:2350. 4. Referenced with permission from the NCCN Clinical Practice Guidelines in Oncology (NCCN Guidelines®) for Colon Cancer V.4.2024. © National Comprehensive Cancer Network, Inc. 2024. All rights reserved. Accessed August 7, 2024. To view the most recent and complete version of the guideline, go online to NCCN.org. 5. Systemic therapy for metastatic colorectal cancer (mCRC) algorithm. ASCO Guidelines®. 2022. 6. Nevala-Plagemann C, Iyengar S, Trunk AD, Pappas L, Haaland B, Garrido-Laguna I. J Natl Compr Canc Netw. 2022;20(3):268-275. 7. Sepulveda AR, Hamilton SR, Allegra CJ, et al. J Clin Oncol. 2017;35:1453-1486. 8. Cervantes A, Adam R, Roselló S, et al. Ann Oncol. 2023;34:10-32. 9. Iyer P, Deng M, Handorf EA, Nakhoda S, Dotan E. JNCI Cancer Spectr. 2022;6:pkac065. 10. Vectibix® (panitumumab) prescribing information, Amgen. 11. El-Deiry WS, Goldberg RM, Lenz HJ, et al. CA Cancer J Clin. 2019;69:305-343. 12. Pennell NA, Arcila ME, Gandara DR, West H. Am Soc Clin Oncol Educ Book. 2019;39:531-542. 13. Mendis S, Beck S, Lee B, et al. Asia Pac J Clin Oncol. 2019;15:136-143.

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