Version July 2025
Dermatologic toxicities occurred in 90% of patients and were severe (National Cancer Institute Common Toxicity Criteria [NCI-CTC] grade 3 and higher) in 15% of patients receiving panitumumab monotherapy.
Dosage guidance:
Safety: Appropriate medical resources for management of severe infusion reactions should be available during panitumumab infusion.
Colorectal cancer, metastatic, RAS wild type: Note: Establish RAS mutation status in colorectal tumors (to confirm RAS wild type [of both KRAS and NRAS]) prior to treatment initiation.
Single agent therapy: IV: 6 mg/kg every 14 days; continue until disease progression or unacceptable toxicity (Ref).
In combination with FOLFOX (fluorouracil, leucovorin, and oxaliplatin): IV: 6 mg/kg every 14 days; continue until disease progression or unacceptable toxicity (Ref). Note: Data from a phase 3 randomized, multicenter trial showed significantly improved overall survival in patients with previously untreated RAS wild-type and left-sided metastatic colorectal cancer who received panitumumab in combination with mFOLFOX6 versus bevacizumab in combination with mFOLFOX6 (Ref). Guidelines from the American Society of Clinical Oncology (ASCO) for the treatment of metastatic colorectal cancer, also recommend the use of an anti-epidermal growth factor receptor agent (eg, panitumumab) plus doublet chemotherapy as first-line treatment in patients with left-sided RAS wild-type metastatic colorectal cancer (Ref).
Off- label combinations:
In combination with CAPOX (capecitabine and oxaliplatin): IV: 9 mg/kg every 21 days; continue for at least 6 cycles or until disease progression or unacceptable toxicity (Ref).
In combination with FOLFIRI (fluorouracil, leucovorin, and irinotecan): IV: 6 mg/kg every 14 days; continue until disease progression or unacceptable toxicity (Ref).
In combination with FOLFOXIRI (fluorouracil, leucovorin, oxaliplatin, and irinotecan): IV: 6 mg/kg every 14 days until disease progression or resection for up to a maximum of 12 preoperative cycles; after resection, patients received the same regimen as adjuvant therapy for a total of 12 perioperative cycles (Ref).
As maintenance therapy (in combination with fluorouracil and leucovorin) following 6 cycles of FOLFOX plus panitumumab): IV: 6 mg/kg every 14 days; continue until disease progression or unacceptable toxicity (Ref).
Colorectal cancer, metastatic, KRAS G12C mutated: Note: Confirm the presence of KRAS G12C mutation prior to treatment initiation. Administer the first sotorasib dose prior to the first panitumumab infusion (Ref).
IV: 6 mg/kg every 14 days (in combination with sotorasib); continue until disease progression or unacceptable toxicity, or until sotorasib is withheld or discontinued (Ref).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling; however, no need for dosage adjustment is expected (Ref).
There are no dosage adjustments provided in the manufacturer's labeling. The following adjustments have been recommended:
Mild or moderate impairment: No dosage adjustment is needed (Ref).
Severe impairment: No need for dosage adjustment is expected (Ref).
American Society of Clinical Oncology guidelines for appropriate systemic therapy dosing in adults with cancer with a BMI ≥30 kg/m2 : The dosing in the FDA-approved prescribing information should be followed in all patients, regardless of obesity status. If a patient with a BMI ≥30 kg/m2 experiences high-grade toxicity from systemic anticancer therapy, the same dosage modification recommendations should be followed for all patients, regardless of obesity status (Ref).
Note: When panitumumab is used in combination with sotorasib, if sotorasib is withheld or permanently discontinued, panitumumab should also be withheld or permanently discontinued. Other concomitant anticancer therapies may also require treatment interruption, dosage reduction, and/or discontinuation.
|
Adverse reaction |
Severity |
Panitumumab dosage modification |
|---|---|---|
|
Dermatologic toxicity (or soft tissue toxicity) |
Grade 3 (first occurrence) |
Withhold panitumumab for 1 to 2 doses; if reaction improves to < grade 3, resume at the original dose. |
|
Grade 3 (second occurrence) |
Withhold panitumumab for 1 to 2 doses; if reaction improves to < grade 3, resume at 80% of the original dose. | |
|
Grade 3 (third occurrence) |
Withhold panitumumab for 1 to 2 doses; if reaction improves to < grade 3, resume at 60% of the original dose. | |
|
Grade 3 (fourth occurrence) |
Permanently discontinue panitumumab. | |
|
Grade 3 that does not recover to < grade 3 after withholding 1 or 2 doses |
Permanently discontinue panitumumab. | |
|
Grade 4 |
Permanently discontinue panitumumab. | |
|
Severe or life-threatening inflammatory or infectious complications |
Withhold or discontinue panitumumab | |
|
Electrolyte depletion (including magnesium, calcium, and potassium) |
Any |
Replete magnesium and other electrolytes as clinically appropriate. |
|
GI toxicity (diarrhea or dehydration) |
Any |
Provide supportive care (including antiemetic or antidiarrheal therapy) as needed; withhold panitumumab as necessary. |
|
Infusion reactions |
Mild to moderate (grade 1 or 2) |
Reduce the infusion rate by 50% for the duration of infusion. |
|
Severe (grade 3 or 4) |
Stop infusion; depending on severity and/or persistence of the reaction, permanently discontinue panitumumab. | |
|
Ocular toxicity: Keratitis, ulcerative keratitis, or corneal perforation |
Acute or worsening |
Interrupt or discontinue panitumumab. |
|
Pulmonary toxicity |
Acute onset or worsening pulmonary symptoms |
Interrupt panitumumab treatment. |
|
Confirmed interstitial lung disease |
Discontinue panitumumab. |
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Reported adverse reactions are for adults.
>10%:
Dermatologic: Acne vulgaris (14%), acneiform eruption (57%), erythema of skin (66%), exfoliative dermatitis (18%), paronychia (25%), pruritus (58%), skin fissure (20%), skin rash (22%), toxicoderma (90%; grades ≥3: 15%)
Endocrine & metabolic: Decreased serum magnesium (38%)
Gastrointestinal: Diarrhea (21%; grades 3/4: 2%), nausea (23%; grades 3/4: <1%), vomiting (19%; grades 3/4: 3%)
Nervous system: Fatigue (26%)
Ophthalmic: Ocular toxicity (16%)
Respiratory: Cough (15%), dyspnea (18%)
Miscellaneous: Fever (17%)
1% to 10%:
Cardiovascular: Pulmonary embolism (1%)
Dermatologic: Dermal ulcer (6%), exfoliation of skin (9%), nail disease (10%), papular rash (2%), pustular rash (4%), xeroderma (10%)
Endocrine & metabolic: Dehydration (3%)
Gastrointestinal: Mucosal swelling (inflammation: 7%), stomatitis (7%), xerostomia (5%)
Hypersensitivity: Infusion-related reaction (3% to 4%)
Immunologic: Antibody development (≤5%; neutralizing: <1%)
Nervous system: Chills (3%)
Ophthalmic: Abnormal eyelash growth (6%), conjunctivitis (5%)
Renal: Acute kidney injury (2%)
Respiratory: Epistaxis (4%), interstitial lung disease (1%)
<1%: Respiratory: Pulmonary fibrosis
Frequency not defined:
Endocrine & metabolic: Hypokalemia
Gastrointestinal: Intestinal obstruction
Postmarketing:
Dermatologic: Bullous skin disease (mucocutaneous), skin necrosis
Hypersensitivity: Angioedema
Ophthalmic: Corneal perforation, keratitis (including ulcerative)
There are no contraindications listed in the manufacturer's US labeling.
Canadian labeling: History of severe or life-threatening hypersensitivity reactions to panitumumab or any component of the formulation.
Concerns related to adverse effects:
• Dermatologic toxicity: Dermatologic toxicities have been reported in most patients receiving panitumumab (as a single agent or in combination other anticancer therapies); severe (≥ grade 3) reactions have occurred; manifestations included dermatitis acneiform, pruritus, erythema, rash, skin exfoliation, paronychia, dry skin, and skin fissures. Severe skin toxicities may be complicated by infection, sepsis, necrotizing fasciitis, or abscesses. The median time to development of skin (or ocular) toxicity was 12 days, with resolution ~14 weeks. The severity of dermatologic toxicity is predictive for response; grades 2 to 4 skin toxicity correlates with improved progression free survival and overall survival, compared to grade 1 skin toxicity (Peeters 2009; Van Cutsem 2007). Rare cases of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) have been reported; bullous mucocutaneous disease (life-threatening/fatal) have been observed. Patients should minimize sunlight exposure and wear sunscreen and protective clothing/hat; sunlight may exacerbate skin reactions.
• Diarrhea: May cause diarrhea; the incidence and severity of chemotherapy-induced diarrhea is increased with combination chemotherapy. Severe diarrhea and dehydration (which may lead to acute kidney failure or other complications) has been observed with panitumumab.
• Electrolyte depletion: Magnesium and/or calcium depletion may occur during treatment; may be delayed. Hypomagnesemia occurred during and for up to 8 weeks after completion of panitumumab treatment. Hypokalemia has also been reported.
• Infusion reactions: Severe infusion reactions (bronchospasm, dyspnea, fever, chills, and hypotension) have been reported in 1% of patients; fatal infusion reactions have been reported with postmarketing surveillance.
• Ocular toxicity: Keratitis, ulcerative keratitis, and corneal perforation have occurred with panitumumab (in combination with chemotherapy or sotorasib).
• Pulmonary toxicity: Pulmonary fibrosis and interstitial lung disease have been observed (rarely) in clinical trials; fatalities have been reported. Patients with a history of or evidence of interstitial pneumonitis or pulmonary fibrosis were excluded from most clinical trials; consider the benefits of therapy versus the risk of pulmonary complications in such patients.
Disease-related concerns:
• Colorectal cancer and RAS mutation status: Confirm absence of RAS mutation prior to treatment; patients with codons 12 and 13 (exon 2), codons 59 and 61 (exon 3), or codons 117 and 146 (exon 4) RAS (KRAS or NRAS) mutations are unlikely to benefit from EGFR inhibitor therapy. The American Society of Clinical Oncology (ASCO) provisional clinical opinion update, as well as a guideline for molecular biomarkers for the evaluation of colorectal cancer, recommend that all patients with metastatic colorectal cancer who are candidates for anti-EGFR therapy should be tested (in a certified lab) for mutations in both KRAS and NRAS exon 2 (codons 12 and 13), exon 3 (codons 59 and 61), and exon 4 (codons 117 and 146); anti-EGFR monoclonal antibody therapy should only be considered in patients whose tumors lack mutations after extended RAS testing (ASCO [Allegra 2016]; ASCP/CAP/AMP/ASCO [Sepulveda 2017]). Information on tests approved for detection of RAS mutation is available at www.fda.gov/CompanionDiagnostics. Panitumumab is also reported to be ineffective in patients with BRAF V600E mutation (Di Nicolantonio 2008).
Concurrent drug therapy issues:
• Bevacizumab and combination chemotherapy: In a study of bevacizumab with combination chemotherapy ± panitumumab, the use of panitumumab resulted in decreased progression-free and overall survival and significantly increased toxicity compared to regimens without panitumumab (Hecht 2009). Toxicities included rash/acneiform dermatitis, diarrhea/dehydration, electrolyte disturbances, mucositis/stomatitis, and an increased incidence of pulmonary embolism.
Special populations:
• Older adult: Patients >65 years of age receiving panitumumab (in combination with FOLFOX) experienced a higher incidence of serious adverse events including severe diarrhea.
Other warnings/precautions:
• Appropriate use: For use as a single agent in metastatic colorectal cancer, assess RAS mutation status in colorectal tumors and confirm the absence of RAS mutation in exon 2 (codons 12 and 13), exon 3 (codons 59 and 61), and exon 4 (codons 117 and 146) of both KRAS and NRAS. For use in combination with sotorasib, confirm the presence of KRAS G12C mutation. Information on tests approved for detection of RAS mutations is available at https://www.fda.gov/CompanionDiagnostics.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous [preservative free]:
Vectibix: 100 mg/5 mL (5 mL); 400 mg/20 mL (20 mL)
No
Solution (Vectibix Intravenous)
100 mg/5 mL (per mL): $434.80
400 mg/20 mL (per mL): $434.80
Disclaimer: A representative AWP (Average Wholesale Price) price or price range is provided as reference price only. A range is provided when more than one manufacturer's AWP price is available and uses the low and high price reported by the manufacturers to determine the range. The pricing data should be used for benchmarking purposes only, and as such should not be used alone to set or adjudicate any prices for reimbursement or purchasing functions or considered to be an exact price for a single product and/or manufacturer. Medi-Span expressly disclaims all warranties of any kind or nature, whether express or implied, and assumes no liability with respect to accuracy of price or price range data published in its solutions. In no event shall Medi-Span be liable for special, indirect, incidental, or consequential damages arising from use of price or price range data. Pricing data is updated monthly.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Solution, Intravenous:
Vectibix: 100 mg/5 mL (5 mL); 400 mg/20 mL (20 mL)
IV: For IV infusion only; do not administer IV push or as a bolus. Doses ≤1,000 mg, infuse over 1 hour; if first infusion is tolerated, subsequent doses may be administered over 30 to 60 minutes. Doses >1,000 mg, infuse over 90 minutes. Administer via infusion pump through a low protein-binding 0.2- or 0.22-micrometer in-line filter through a peripheral IV line or indwelling catheter. Flush line with NS before and after infusion; do not mix or administer with other medications.
When used in combination with sotorasib, administer the first sotorasib dose prior to the first panitumumab infusion.
Reduce infusion rate by 50% for mild to moderate infusion reactions (grades 1 and 2); stop infusion for severe infusion reactions (grades 3 and 4) and consider permanent discontinuation. Appropriate medical support for the management of infusion reactions should be readily available.
Colorectal cancer, metastatic, RAS wild-type:
First-line treatment (combination with FOLFOX [fluorouracil, leucovorin, and oxaliplatin]) of wild-type RAS (defined as wild-type in both KRAS and NRAS as determined by an approved test) metastatic colorectal cancer (mCRC) in adults.
Treatment (as a single agent) of wild-type RAS (defined as wild-type in both KRAS and NRAS as determined by an approved test) mCRC in adults following disease progression after prior treatment with fluoropyrimidine-, oxaliplatin-, and irinotecan-containing chemotherapy.
Colorectal cancer, metastatic, KRAS G12C-mutated: Treatment (in combination with sotorasib) of KRAS G12C-mutated mCRC (as determined by an approved test) in adults who have received prior fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy.
Limitations of use: Panitumumab is not indicated for the treatment of patients with RAS-mutant mCRC (unless used in combination with sotorasib in KRAS G12C-mutated mCRC), or for the treatment of patients with mCRC in whom RAS mutation status is unknown.
Cutaneous squamous cell carcinoma, unresectable, advanced or metastatic
Panitumumab may be confused with pembrolizumab, pertuzumab, polatuzumab vedotin
The Institute for Safe Medication Practices (ISMP) includes this medication among its list of drug classes (chemotherapeutic agent, parenteral and oral) which have a heightened risk of causing significant patient harm when used in error (High-Alert Medications in Acute Care, Community/Ambulatory Care, and Long-Term Care Settings).
None known.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the drug interactions program by clicking on the “Launch drug interactions program” link above.
Aminolevulinic Acid (Systemic): Photosensitizing Agents may increase photosensitizing effects of Aminolevulinic Acid (Systemic). Risk X: Avoid
Aminolevulinic Acid (Topical): Photosensitizing Agents may increase photosensitizing effects of Aminolevulinic Acid (Topical). Risk C: Monitor
Efgartigimod Alfa: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Methoxsalen (Systemic): Photosensitizing Agents may increase photosensitizing effects of Methoxsalen (Systemic). Risk C: Monitor
Nipocalimab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Porfimer: Photosensitizing Agents may increase photosensitizing effects of Porfimer. Risk X: Avoid
Rozanolixizumab: May decrease therapeutic effects of Fc Receptor-Binding Agents. Risk C: Monitor
Verteporfin: Photosensitizing Agents may increase photosensitizing effects of Verteporfin. Risk C: Monitor
Patients who could become pregnant should use effective contraception during treatment and for 2 months after the dose of panitumumab.
Based on animal reproduction studies and on the mechanism of action, panitumumab may cause fetal harm if administered during pregnancy. Panitumumab is a humanized monoclonal antibody (IgG2). Potential placental transfer of human IgG is dependent upon the IgG subclass and gestational age, generally increasing as pregnancy progresses. The lowest exposure would be expected during the period of organogenesis (Palmeira 2012; Pentsuk 2009).
It is not known if panitumumab is present in breast milk.
Panitumumab is an IgG monoclonal antibody and maternal IgG immunoglobulins are excreted in breast milk; however, breast milk antibodies are not expected to enter neonatal and infant circulation in substantial amounts. Due to the potential for serious adverse reactions in the breastfeeding infant, the manufacturer recommends patients not breastfeed during therapy and for 2 months after the final panitumumab dose.
RAS genotyping of tumor tissue to confirm RAS wild-type (prior to treatment initiation) or KRAS G12C mutation status (in tumor specimens; if using in combination with sotorasib). Monitor serum electrolytes, including magnesium and calcium (periodically during and for at least 8 weeks after therapy), and potassium. Monitor vital signs and temperature before, during, and after infusion; monitor for signs/symptoms of infusion reaction. Monitor all dermatologic toxicities for development of inflammation or infection. Monitor for signs/symptoms of ocular toxicity (eg, keratitis, ulcerative keratitis, or corneal perforation), and for acute onset or worsening pulmonary symptoms.
The American Society of Clinical Oncology hepatitis B virus (HBV) screening and management provisional clinical opinion (ASCO [Hwang 2020]) recommends HBV screening with hepatitis B surface antigen, hepatitis B core antibody, total Ig or IgG, and antibody to hepatitis B surface antigen prior to beginning (or at the beginning of) systemic anticancer therapy; do not delay treatment for screening/results. Detection of chronic or past HBV infection requires a risk assessment to determine antiviral prophylaxis requirements, monitoring, and follow-up.
Cardiovascular monitoring: Comprehensive assessment prior to treatment including a history and physical examination, screening for cardiovascular disease risk factors such as hypertension, diabetes, dyslipidemia, obesity, and smoking (ASCO [Armenian 2017]; ESC [Lyon 2022]).
Panitumumab is a recombinant human IgG2 monoclonal antibody which binds specifically to the epidermal growth factor receptor (EGFR, HER1, c-ErbB-1) and competitively inhibits the binding of epidermal growth factor (EGF) and other ligands. Binding to the EGFR blocks phosphorylation and activation of intracellular tyrosine kinases, resulting in inhibition of cell survival, growth, proliferation, and transformation. EGFR signal transduction may result in KRAS and NRAS wild-type activation; cells with RAS mutations appear to be unaffected by EGFR inhibition. In KRAS G12C-mutant metastatic colorectal cancer, EGFR activation is a resistance mechanism for KRAS G12C inhibition. In animal colorectal tumor models, the combination of panitumumab and sotorasib demonstrated increased antitumor activity compared to either agent alone.
Half-life elimination: ~7.5 days (range: ~4 to ~11 days).
Excretion: Clearance (mean): 4.9 ± 1.4 mL/kg/day.
