Pemigatinib, a potent and selective small-molecule inhibitor of fibroblast growth factor (FGF) receptors (FGFR1, FGFR2, and FGFR3), is an antineoplastic agent.4
Pemigatinib is used 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.1 The accelerated approval of pemigatinib for this indication is based on overall response rate and duration of response.1 Continued approval for this indication may be contingent on verification and description of clinical benefit of pemigatinib in confirmatory studies.1 The drug has been designated an orphan drug by FDA for the treatment of cholangiocarcinoma.5 An FDA-approved companion diagnostic test is required to confirm the presence of an FGFR2 fusion or rearrangement prior to initiation of pemigatinib therapy.1
This indication for pemigatinib for the treatment of cholangiocarcinoma is based principally on the results of an open-label, multicenter, noncomparative, phase 2 study (FIGHT-202) in a cohort of 107 patients with unresectable locally advanced or metastatic cholangiocarcinoma harboring an FGFR2 genomic aberration.1, 2 In this cohort, FGFR2 genomic aberrations included in-frame gene fusions and other gene rearrangements predicted to have a breakpoint within intron 17/exon 18 of the FGFR2 gene and an intact FGFR2 kinase domain.1 Patients were eligible for this study if they experienced disease progression during or following at least one prior chemotherapy.1 In this study, patients received pemigatinib 13.5 mg orally once daily on days 1-14 of each 21-day cycle.1, 2 Pemigatinib therapy was continued until disease progression or unacceptable toxicity occurred.1 The median age of patients enrolled in this study was 56 years (range: 26-77 years); 98% of patients had intrahepatic cholangiocarcinoma, 61% were female, 74% were white, and 95% had an Eastern Cooperative Group (ECOG) performance status of 0 or 1.1 Approximately one-third (27%) of patients had received 2 prior systemic therapies and 12% had received 3 or more prior lines of therapy.1 Most patients had previously received platinum-based chemotherapy immediately prior to study enrollment; the most commonly used platinum-based regimen was gemcitabine and cisplatin combination therapy.2 Most patients (86%) had in-frame FGFR gene fusions and 14% of patients had FGFR2 gene rearrangements that could not be confidently predicted to be in-frame fusions (e.g., rearrangements without an identifiable partner gene); the most commonly identified FGFR2 gene fusion was FGFR2-BICC1 (34%).1
At a median follow-up of 15.4 months in the cohort of patients with FGFR2 genomic aberrations, the objective response rate was 36%; complete response (CR) was achieved in 2.8% of patients.1, 2 The median duration of CR was 9.1 months; 63 or 18% of patients had durable responses of 6 or 12 months or longer, respectively.1 The median time to CR was 2.7 months.1, 2 At the time of data analysis, median progression-free survival or overall survival was 6.9 or 21.1 months, respectively; however, overall survival data were not mature at the time of analysis.2 In the cohort of patients with FGFR2 genomic aberrations, results of a subgroup analysis suggested that the effect of pemigatinib on objective response was consistent across all demographic and disease subgroups.2
Pemigatinib is used for the treatment of adults with relapsed or refractory myeloid/lymphoid neoplasms with fibroblast growth factor receptor 1 ( FGFR1 ) rearrangement.1 The drug has been designated an orphan drug by FDA for the treatment of certain types of myeloid/lymphoid neoplasms.5 Patients should be selected for treatment based on the presence of an FGFR1 rearrangement; an FDA-approved test for detection of an FGFR1 rearrangement in patients with relapsed or refractory myeloid//lymphoid neoplasm is not available.1
This indication for pemigatinib for the treatment of myeloid/lymphoid neoplasms with FGFR1 rearrangement is based principally on the results of an open-label, multicenter, single-arm study (FIGHT-203) in a cohort of 28 patients with documented myeloid/lymphoid neoplasms with 8p11 rearrangement shown to be an FGFR1 activating mutation.1 Patients could have relapsed after allogeneic hematopoietic stem cell transplantation (HSCT) or disease-modifying therapy, or were not a candidate for allogeneic HSCT or other disease-modifying therapies.1
In this study, patients received pemagitinib 13.5 mg once daily in 21-day cycles, either continuously or intermittently (14 days on, 7 days off).1 Pemagitinib therapy was continued until disease progression, unacceptable toxicity, or until patients were able to receive an allogeneic HSCT.1 The median age of patients enrolled in the study was 65 years (range: 39-78 years); 64% were female, 68% were white, 3.6% were Black or African American, 11% were Asian, 3.6% were American Indian/Alaska Native, 3.6% were Hispanic, and 88% had an ECOG performance status of 0 or 1.1
In patients with chronic phase in the marrow with or without extramedullary disease (n=18), efficacy was established based on CR.1 In these patients, CR rate was 78% and median time to CR was 104 days (range: 44 to 435 days).1 The median duration of CR was not reached at the time of analysis.1 In patients with blast phase in the marrow with or without extramedullary disease (n=4), two patients achieved CR.1 In patients with extramedullary disease only (n=3), one patient achieved CR.1 For all 28 patients in the study cohort, the complete cytogenetic response rate was 79%.1
Pemigatinib is administered orally once daily without regard to food at approximately the same time of day.1 The tablets should be swallowed whole and should not be split, crushed, chewed, or dissolved.1
If a dose of pemigatinib is missed and cannot be taken within 4 hours or if vomiting occurs, the missed or vomited dose should be skipped and the next dose should be taken at the regularly scheduled time.1
The tablets should be stored at 20-25°C (excursions permitted between 15-30°C).1
For the treatment of previously treated, unresectable locally advanced or metastatic cholangiocarcinoma with FGFR2 fusion or rearrangement in adults, the recommended dosage of pemigatinib is 13.5 mg once daily on days 1-14 of each 21-day cycle.1 Therapy should be continued until disease progression or unacceptable toxicity occurs.1
For the treatment of relapsed or refractory myeloid/lymphoid neoplasms with FGFR1 rearrangement in adults, the recommended dosage of pemigatinib is 13.5 mg once daily on a continuous basis.1 Therapy should be continued until disease progression or unacceptable toxicity occur.1
Dosage Modification for Toxicity
Temporary interruption of therapy, dosage reduction, and/or permanent discontinuance of pemigatinib may be necessary in patients experiencing certain adverse effects.1 When dosage modification of pemigatinib is necessary, the dosage of pemigatinib should be reduced as described in Table 1.1
Dosage Reduction Level | Recommended Dosage (Initial Dose = 13.5 mg once daily on days 1-14 of each 21-day cycle) | Recommended Dosage (Initial Dose = 13.5 mg once daily on a continuous basis) |
|---|---|---|
First | Resume at 9 mg once daily on days 1-14 of each 21-day cycle | 9 mg once daily |
Second | Resume at 4.5 mg once daily on days 1-14 of each 21-day cycle | 4.5 mg once daily |
Third | Permanently discontinue drug | 4.5 mg once daily for first 14 days of each 21-day cyclea |
aPermanently discontinue if unable to tolerate 4.5 mg once daily for 14 days of each 21-day cycle.
If retinal pigment epithelial detachment occurs, temporary interruption of therapy, dosage reduction, and/or permanent discontinuance of the drug as described in Table 2 may be necessary.1
Severity | Dosage Modification |
|---|---|
Asymptomatic and stable on serial eye exams | Continue pemigatinib therapy |
Symptomatic or worsening on serial eye exams | Withhold therapy |
If symptoms resolve or signs of retinal pigment epithelial detachment improve on subsequent eye exams; reduce dosage (see Table 1) | |
If the toxicity does not resolve or improve on examination, consider permanent discontinuance of drug based on clinical status |
If hyperphosphatemia occurs, temporary interruption of therapy, dosage reduction, and/or permanent discontinuance of the drug as described in Table 3 may be necessary.1
Serum Phosphate Concentration (mg/dL) | Dosage Modification |
|---|---|
>7 to ≤10 | Initiate phosphate lowering therapy and monitor serum phosphate concentrations weekly |
First occurrence: Withhold therapy if serum phosphate concentrations do not improve to <7 mg/dL within 2 weeks of initiating phosphate lowering therapy; resume therapy at same dosage when serum phosphate concentrations improve to <7 mg/dL | |
Subsequent occurrences: Withhold therapy if serum phosphate concentrations do not improve to <7 mg/dL within 2 weeks of initiating phosphate lowering therapy; resume therapy at reduced dosage when serum phosphate concentrations improve to <7 mg/dL (see Table 1) | |
>10 | Initiate phosphate lowering therapy and monitor serum phosphate concentrations weekly |
Withhold therapy if serum phosphate concentrations do not improve to ≤10 mg/dL within 1 week of initiating phosphate lowering therapy; resume at next lower dosage level when serum phosphate concentrations improve to <7 mg/dL (see Table 1) | |
If serum phosphate concentrations >10 mg/dL recur following 2 levels of dosage reduction, permanently discontinue drug |
If other grade 3 adverse reactions occur, pemigatinib therapy should be withheld for 2 weeks; therapy may be resumed at a dosage reduced by 1 dose level when the toxicity improves to grade 1 or baseline.1 (See Table 1.)
If the grade 3 adverse reaction does not improve within 2 weeks of withholding therapy, pemigatinib therapy should be permanently discontinued.1
If grade 4 adverse reactions occur, pemigatinib therapy should be permanently discontinued.1
Concomitant Use with CYP3A Inhibitors
Concomitant use of pemigatinib with strong or moderate inhibitors of cytochrome P-450 (CYP) isoenzyme 3A should be avoided.1 If concomitant use of a strong or moderate CYP3A inhibitor cannot be avoided, the manufacturer recommends reducing the dosage of pemigatinib by 4.5 mg (e.g., from 13.5 mg to 9 mg once daily, from 9 mg to 4.5 mg once daily).1 If concomitant use of the strong or moderate CYP3A inhibitor is discontinued, the pemigatinib dosage should be returned (after 3 elimination half-lives of the CYP3A inhibitor) to the dosage used prior to initiation of the CYP3A inhibitor.1
In patients with severe hepatic impairment (total bilirubin concentration >3 times the upper limit of normal [ULN] with any AST concentration), reduce pemigatinib dosage to 9 mg with the schedule (intermittent or continuous) designated for the indication for use.1
No dosage adjustment is necessary in patients with mild (total bilirubin concentration 1-1.5 times the ULN or AST concentration exceeding the ULN) or moderate (total bilirubin concentration 1.5-3 times the ULN with any AST concentration) hepatic impairment.1
In patients with severe renal impairment (glomerular filtration rate [GFR] 15-29 mL/minute per 1.73 m2 estimated by the Modification of Diet in Renal Disease [MDRD] equation), reduce pemigatinib dosage to 9 mg with the schedule (intermittent or continuous) designated for the indication for use.1
No dosage adjustment is necessary in patients with mild or moderate renal impairment (GFR 30-89 mL/minute).1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
Retinal pigment epithelial detachment resulting in blurred vision, visual floaters, or photopsia has been reported in patients receiving pemigatinib.1 In clinical trials, retinal pigment epithelial detachment occurred in 11% of patients receiving a starting dose of pemigatinib 13.5 mg and was grade 3 or 4 in 1.3% of patients receiving the drug.1 The median time to initial onset of retinal pigment epithelial detachment was 56 days.1 Temporary interruption, dosage reduction, or permanent discontinuance of pemigatinib therapy was necessary because of retinal pigment epithelial detachment in 3.1, 1.3, or 0.2%, respectively, of patients receiving the drug.1 Retinal pigment epithelial detachment resolved or improved to grade 1 in 76% of patients who required dosage modification.1 The incidence of asymptomatic retinal pigment epithelial detachment is unknown.1 Ophthalmologic examination, including optical coherence tomography, was not performed routinely in clinical trials.1
Dry eye symptoms also have occurred in 31% of patients and were grade 3-4 in 1.6% of patients receiving a starting dose of pemigatinib 13.5 mg across clinical trials.1 Ocular demulcents should be administered as needed for the management of dry eye symptoms.1, 9
Ophthalmologic examinations, including optical coherence tomography, should be performed prior to initiation of pemigatinib, every 2 months during the first 6 months of therapy, and then every 3 months thereafter.1 If visual disturbances are reported, ophthalmologic examinations should be performed urgently with follow-up every 3 weeks until resolution of symptoms or discontinuation of pemigatinib therapy.1 Temporary interruption, dosage reduction, or discontinuance of pemigatinib may be necessary if ocular toxicities occur during therapy with the drug.1
Hyperphosphatemia and Soft Tissue Mineralization
Pemigatinib can cause hyperphosphatemia leading to soft tissue mineralization, cutaneous calcification, calcinosis, and nonuremic calciphylaxis.1 Increased serum phosphate concentration is a consequence of inhibition of fibroblast growth factor receptor (FGFR).1 In clinical trials, hyperphosphatemia was reported in 93% of patients receiving a starting dose of pemigatinib 13.5 mg.1 The median time to onset of hyperphosphatemia was 8 days (range: 1-169 days) following initiation of pemigatinib.1 Phosphate lowering therapy was required in 33% of patients receiving pemigatinib.1 In the primary efficacy study for cholangiocarcinoma, hyperphosphatemia was managed with a low-phosphate diet, phosphate binders, diuretic therapy, or dosage reduction or interruption.2
Serum phosphate concentrations should be monitored during pemigatinib therapy.1 A low-phosphate diet should be initiated in patients with serum phosphate concentrations exceeding 5.5 mg/dL.1 If serum phosphate concentrations exceed 7 mg/dL, phosphate lowering therapy should be initiated, and temporary interruption of therapy, dosage reduction, and/or permanent discontinuance of pemigatinib therapy may be necessary.1
Pemigatinib may cause fetal harm in humans based on its mechanism of action and animal findings; embryofetal toxicity and teratogenicity have been demonstrated in animals.1
There are no data regarding use of pemigatinib in pregnant females.1 In animal reproduction studies, embryofetal toxicity (i.e., postimplantation loss, reduced fetal body weight, growth retardation) and teratogenic effects (i.e., skeletal and visceral anomalies, major blood vessel variations, reduced ossification) were observed in rats receiving pemigatinib at maternal exposure levels as low as approximately 0.2 times the human exposure levels at the maximum recommended human dose.1
Pregnancy should be avoided during pemigatinib therapy.1 The manufacturer recommends confirmation of pregnancy status prior to initiation of pemigatinib in females of reproductive potential and states that such females be advised to use effective contraceptive methods while receiving pemigatinib and for 1 week after the final dose.1 In addition, men with such female partners should use effective methods of contraception while receiving pemigatinib and for 1 week after the final dose.1 Patients should be apprised of the potential hazard to the fetus if pemigatinib is used during pregnancy.1
Pemigatinib may cause fetal harm if administered to pregnant females based on its mechanism of action and animal findings.1
It is not known whether pemigatinib or its metabolites are distributed into human milk.1 The effects of the drug on nursing infants or on the production of milk are unknown.1
Because of the potential for adverse reactions to pemigatinib in nursing infants, females should be advised not to nurse while receiving the drug and for 1 week after the final dose.1
Females and Males of Reproductive Potential
Verify pregnancy status of females of reproductive potential prior to pemigatinib therapy.1 Advise females of reproductive potential to use effective contraception during treatment with pemigatinib and for 1 week following the last dose of the drug.1
Advise males with female partners of reproductive potential to use effective contraception during treatment with pemigatinib and for 1 week following the last dose of the drug.1
Safety and efficacy of pemigatinib have not been established in pediatric patients.1
In animal toxicology studies, pemigatinib has been associated with changes in growing teeth (complete loss of ameloblasts with associated secondary changes) and bones (physeal and cartilage dysplasia).1 Complete recovery was not observed 6 weeks after the last dose.1 In a 13-week study, misaligned, whitened, broken, and trimmed/thinned incisors also were reported.1
In the principal efficacy study evaluating pemigatinib in patients with previously treated locally advanced or metastatic cholangiocarcinoma, 32% of patients were 65 years of age or older and 8% were 75 years of age or older.1 In the principal efficacy study evaluating pemigatinib in patients with myeloid/lymphoid neoplasms, 44% of patients were 65 years of age or older and 2.9% were 75 years of age or older.1 No clinically important differences in safety or efficacy were observed between geriatric patients and younger adults.1
Pharmacokinetics of pemigatinib do not appear to be altered in patients with mild (total bilirubin concentrations >1-1.5 times the upper limit of normal [ULN] or AST concentration exceeding the ULN) to moderate (total bilirubin concentration >1.5-3 times the ULN with any AST concentration) hepatic impairment.1
Pemigatinib exposure is increased by 136% in patients with severe hepatic impairment (total bilirubin concentration >3 times the ULN with any AST concentration); dosage adjustment is recommended.1
Pharmacokinetics of pemigatinib do not appear to be altered in patients with mild to moderate renal impairment (glomerular filtration rate [GFR] 30-89 mL/minute per 1.73 m2 estimated by the Modification of Diet in Renal Disease [MDRD] equation) or in patients with end-stage renal disease (GFR <15 mL/minute per 1.73 m2) requiring intermittent hemodialysis.1
Pemigatinib exposure is increased by 59% in patients with severe renal impairment (GFR 15-29 mL/minute per 1.73 m2); dosage adjustment is recommended.1
Pemigatinib has been shown to increase serum creatinine concentrations, but may not affect GFR.1 Pemigatinib decreases tubular secretion of creatinine by inhibiting renal organic cation transporter (OCT) 2 and multidrug and toxin extrusion transporter (MATE) 1.1 In the primary efficacy study, the mean increase in serum creatinine concentrations was 0.2 mg/dL.1 Elevated concentrations of serum creatinine reached steady state by day 8 of cycle 1 and decreased during the treatment-free period (days 15-21).1 The manufacturer states that parameters not based on serum creatinine concentrations should be considered to evaluate renal function if elevated serum creatinine concentrations persist.1
Adverse reactions reported in 20% or more of patients with cholangiocarcinoma receiving pemigatinib include hyperphosphatemia, alopecia, diarrhea, nail toxicity, fatigue, dysgeusia, nausea, constipation, stomatitis, dry eyes, dry mouth, decreased appetite, vomiting, arthralgia, abdominal pain, hypophosphatemia, back pain, and dry skin.1
Adverse reactions reported in 20% or more of patients with myeloid/lymphoid neoplasms receiving pemigatinib include hyperphosphatemia, alopecia, diarrhea, nail toxicity, fatigue, nausea, constipation, stomatitis, dry eyes, dry mouth, decreased appetitie, abdominal pain, back pain, dry skin, rash, anemia, epistaxis, serous retinal detachment, extremity pain, dyspepsia, back pain, blurred vision, peripheral edema, and dizziness.1
Pemigatinib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A4.1 In vitro, pemigatinib is not an inhibitor of CYP isoenzymes 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, or 3A4 or an inducer of CYP isoenzymes 1A2, 2B6, or 3A4.1
In vitro studies indicate that pemigatinib is a substrate of P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP).1 In vitro, pemigatinib is an inhibitor of P-gp, organic cation transporter (OCT) 2, and multidrug and toxin extrusion (MATE) 1.1
Drugs Affecting Hepatic Microsomal Enzymes
Concomitant use of pemigatinib with strong or moderate inhibitors of CYP3A may result in increased systemic exposure of pemigatinib and an increased incidence or severity of adverse effects.1 When the strong CYP3A inhibitor itraconazole was administered concomitantly with pemigatinib (single 4.5-mg dose), the AUC or peak plasma concentration of pemigatinib increased by 88 or 17%, respectively.1 Simulations using physiologically based pharmacokinetic models suggest that moderate CYP3A inhibitors may increase the systemic exposure of pemigatinib by approximately 50-80%.1
Concomitant use of pemigatinib with strong or moderate CYP3A inhibitors should be avoided.1 If concomitant use of a strong or moderate CYP3A inhibitor cannot be avoided, the manufacturer recommends reducing the dosage of pemigatinib by 4.5 mg (e.g., from 13.5 mg to 9 mg once daily, from 9 mg to 4.5 mg once daily).1 If concomitant use of the strong or moderate CYP3A inhibitor is discontinued, the pemigatinib dosage should be returned (after 3 elimination half-lives of the CYP3A inhibitor) to the dosage used prior to initiation of the CYP3A inhibitor.1
Concomitant use of pemigatinib with strong or moderate inducers of CYP3A may result in decreased pemigatinib plasma concentrations and reduced pemigatinib efficacy.1 When the strong CYP3A inducer rifampin was administered concomitantly with pemigatinib (single 13.5-mg dose), the AUC or peak plasma concentration of pemigatinib decreased by 85 or 62%, respectively.1
Concomitant use of pemigatinib with strong or moderate CYP3A inducers should be avoided.1
When the proton-pump inhibitor esomeprazole was administered concomitantly with pemigatinib, no clinically important effect on systemic exposure of pemigatinib was observed.1
Concomitant administration of pemigatinib with the histamine H2-receptor antagonist ranitidine did not have a clinically important effect on systemic exposure to pemigatinib.1
Drugs Affecting or Affected by Transport Systems
Concomitant use of pemigatinib with inhibitors of P-gp or BCRP are not expected to affect systemic exposure of pemigatinib at clinically relevant concentrations.1
When pemigatinib was coadministered with the OCT2 and MATE1 substrate metformin, no clinically important changes in blood glucose concentration was observed.1
Pemigatinib, a potent and selective inhibitor of fibroblast growth factor receptors (FGFR)1, FGFR2, and FGFR3, is an antineoplastic agent.1, 2, 6 Similar to other receptor tyrosine kinases, activation of FGFR tyrosine kinase is involved in the initiation of various cascades of intracellular signaling events leading to cell proliferation and influences processes critical to cell survival and tumor progression (e.g., angiogenesis, metastasis, inhibition of apoptosis).7, 8 Aberrations in FGFR (e.g., gene amplification, point mutation, chromosomal translocation) resulting in dysregulation of the FGFR signaling cascade have been implicated in various solid tumors;6, 7 FGFR2 gene fusions and rearrangements have been identified in 10-20% of patients with intrahepatic cholangiocarcinoma.2, 8 Binding of pemigatinib to FGFR1, FGFR2, and FGFR3 results in inhibition of constitutive FGFR signaling and reduced cell viability in cell lines expressing aberrant FGFR.1 In vitro, pemigatinib demonstrated antitumor activity in mice bearing human tumor xenografts harboring FGFR1 , FGFR2 , or FGFR3 genomic aberrations, including cholangiocarcinoma that expressed the FGFR-2-Transformer-2 beta homolog (TRA2b) fusion protein.1 Pemigatinib also has demonstrated inhibition of FGFR4 with a half-maximal inhibitory concentration approximately 100 times higher than the half-maximal inhibitory concentration for FGFR1, FGFR2, or FGFR3.1, 8
Serum phosphate concentration is a marker of FGFR inhibition following initiation of pemigatinib therapy.1 The increase in serum phosphate is concentration-dependent across the dosage range of 1-20 mg once daily.1
Steady-state concentration of pemigatinib is dose proportional over the dosage range of 1-20 mg.1 The median time to peak plasma concentration of pemigatinib is 1.13 hours.1 Steady-state concentrations of pemigatinib are reached after 4 days of once-daily dosing and the median accumulation ratio is 1.63.1 Administration of pemigatinib with a high-fat, high-calorie meal (approximately 1000 calories with approximately 50% of calories from fat) did not have a clinically meaningful effect on the pharmacokinetics of pemigatinib.1
Pemigatinib is metabolized principally by cytochrome P-450 (CYP) isoenzymes 3A4.1 Pemigatinib is highly bound (90.6%) to plasma proteins in vitro and is independent of drug concentration.1 The mean elimination half-life of pemigatinib is 15.4 hours.1 Following administration of a single oral radiolabeled dose of pemigatinib, 82.4% of the recovered dose is excreted in feces (1.4% as unchanged drug) and 12.6% is eliminated in urine (1% as unchanged drug).1 Clearance of pemigatinib does not appear to be affected by age (range: 21-79 years), sex, race, or body weight (range: 40-156 kg).1
Additional Information
The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer's labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care. For further information on the handling of antineoplastic agents, see the ASHP Guidelines on Handling Hazardous Drugs at [Web].
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Pemigatinib is available only from a designated specialty pharmacy.3 The manufacturer should be contacted for additional information.3
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablet | 4.5 mg | Incyte | |
9 mg | Pemazyre® | Incyte | ||
13.5 mg | Pemazyre® | Incyte |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions September 10, 2024. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
1. Incyte Corporation. Pemazyre® (pemigatinib) tablets prescribing information. Wilmington, DE; 2023 Jun.
2. Abou-Alfa GK, Sahai V, Hollebecque A et al. Pemigatinib for previously treated, locally advanced or metastatic cholangiocarcinoma: a multicentre, open-label, phase 2 study. Lancet Oncol . 2020; 21:671-684. [PubMed 32203698]
3. Incyte Corporation. Pemazyre® Access and Support. Accessed 2024 Jun 24. From Pemazyre® for US Healthcare Professionals website. [Web]
4. Bekaii-Saab TS, Valle JW, Cutsem EV et al. FIGHT-302: first-line pemigatinib vs gemcitabine plus cisplatin for advanced cholangiocarcinoma with FGFR2 rearrangements. Future Oncol . 2020; 16:2385-2399. [PubMed 32677452]
5. Food and Drug Administration. FDA Application: Search orphan drug designations and approvals. Silver Spring, MD. From FDA web site. [Web]
6. Liu PCC, Koblish H, Wu L et al. INCB054828 (pemigatinib), a potent and selective inhibitor of fibroblast growth factor receptors 1, 2, and 3, displays activity against genetically defined tumor models. PLoS One . 2020; 15:e0231877. [PubMed 32315352]
7. Dai S, Zhou Z, Chen Z et al. Fibroblast Growth Factor Receptors (FGFRs): Structures and Small Molecule Inhibitors. Cells . 2019; 8 [PubMed 31216761]
8. Food and Drug Administration. Center for Drug Evaluation and Research. Application number: 213736Orig1s000: Multi-discipline review. From FDA website [Web]
9. Vinson KB, Gillette WM, Baston CF et al. Trichiasis and dry eye syndrome in two patients on novel fibroblast growth factor receptor inhibitor therapies. Am J Ophthalmol Case Rep . 2020; 19:100818. [PubMed 32695928]