Fruquintinib, a small molecule kinase inhibitor of vascular endothelial growth factor (VEGF) receptors 1, 2, and 3, is an antineoplastic agent.1
Fruquintinib is used for the treatment of metastatic colorectal cancer in adults who previously received fluoropyrimidine-, oxaliplatin-, and irinotecan-containing regimens; an anti-VEGF therapy; and, in those with tumors bearing the wild-type (nonmutated) RAS genes, and when medically appropriate, an epidermal growth factor receptor inhibitor (anti-EGFR therapy).1
Efficacy of fruquintinib for this use is based principally on the results of 2 randomized controlled studies (FRESCO-2 and FRESCO).1, 2, 3
FRESCO-2 was a randomized, double-blind, placebo-controlled, phase 3 study in 691 patients with previously treated metastatic colorectal cancer.1, 2 Patients enrolled had disease progression during or after prior treatment with fluoropyrimidine-, oxaliplatin-, irinotecan-based chemotherapy; an anti-VEGF biological therapy; an anti-EGFR biological therapy (in those with tumors bearing the wild-type RAS genes); and trifluridine/tipiracil, regorafenib, or both.1, 2 Patients were randomized (stratified by prior use of trifluridine/tipiracil or regorafenib, RAS mutation status, and duration of metastatic disease) in a 2:1 ratio to receive either fruquintinib (5 mg orally once daily) or placebo for the first 21 days of each 28-day cycle, with best supportive care.1, 2 Treatment was continued until disease progression, death, unacceptable toxicity, or discontinuation of treatment for other reasons.2 The primary measure of efficacy was overall survival.1, 2
The median age of patients in FRESCO-2 was 64 years; 56% were male, 81% were white, and 63% had RAS -mutant tumors.1, 2 Patients in the study had previously received a median of 4 lines of systemic therapy for metastatic disease.2 There were 96% of patients who received prior anti-VEGF therapy and 39% of patients who received prior anti-EGFR therapy.1, 2 In addition, all patients received previous treatment with either trifluridine/tipiracil (52%), regorafenib (8%), or both trifluridine/tipiracil and regorafenib (39%).2
In FRESCO-2, the median duration of treatment was 3.1 months and 1.8 months for patients who received fruquintinib and placebo, respectively.2 Patients receiving fruquintinib had a longer median overall survival compared to those receiving placebo (7.4 versus 4.8 months) and longer progression-free survival (3.7 versus 1.8 months).1, 2
FRESCO was a randomized, double-blind, placebo-controlled, phase 3 study in 416 patients with previously treated metastatic colorectal cancer.1, 3 Patients enrolled had disease progression during or after prior treatment with fluoropyrimidine-, oxaliplatin-, or irinotecan-based chemotherapy.1, 3 Patients were randomized (stratified by prior use of anti-VEGF therapy and KRAS mutation status) in a 2:1 ratio to receive either fruquintinib (5 mg orally once daily) or placebo for the first 21 days of each 28-day cycle, with best supportive care.1, 3 Treatment was continued until disease progression, death, unacceptable toxicity, or discontinuation of treatment for other reasons.3 The primary measure of efficacy was overall survival.1, 3
The median age of patients in FRESCO was 56 years; 61% were male, 100% were Asian, and 44% had KRAS -mutant tumors.1 There were 30% of patients who received prior anti-VEGF therapy and 14% of patients who received prior anti-EGFR therapy.1
In FRESCO, the median time of follow-up was 13.3 months and 13.2 months for patients who received fruquintinib and placebo, respectively.3 Patients receiving fruquintinib had a longer median overall survival compared to those receiving placebo (9.3 versus 6.6 months) and longer progression-free survival (3.7 versus 1.8 months).1, 3
The American Society of Clinical Oncology (ASCO) guidelines for metastatic colorectal cancer and late-stage colorectal cancer do not discuss the specific place in therapy for fruquintinib.17, 18
The ASCO guideline for the treatment of patients with late-stage colorectal cancer generally recommends doublet or triplet fluoropyrimidine-based chemotherapy with or without bevacizumab regardless of mutation status; however, patients with wild-type and certain comorbidities or risk factors who are not candidates for chemotherapy may be offered monotherapy with anti-EGFR therapy (e.g., cetuximab, panitumumab).17 Immune checkpoint inhibitors (e.g., pembrolizumab, nivolumab, nivolumab in combination with ipilimumab) may also be considered in patients with deficient mismatch repair (dMMR) or high microsatellite instability (MSI-H) colorectal cancer (regardless of mutation status) who are not candidates for intensive chemotherapy.17
First-line treatment options for patients with late-stage colorectal cancer are the same regardless of whether the intent is curative or palliative.17 Second-line treatment options for the treatment of metastatic colorectal cancer include immune checkpoint inhibitors or chemotherapy with or without anti-EGFR therapy or ziv-aflibercept, and should be chosen based on the regimen used in the first-line setting (e.g., bevacizumab, oxaliplatin, irinotecan) and disease characteristics (e.g., RAS or BRAF mutation status, dMMR, microsatellite instability [MSI] status).17 ASCO states that regorafenib or trifluridine/tipiracil may be considered in the third- or fourth-line setting in patients with any RAS/BRAF status; however, the drugs are recommended in patients with metastatic colorectal cancer harboring wild-type RAS who were previously treated with fluoropyrimidines, oxaliplatin, irinotecan, bevacizumab, and anti-EGFR therapy.17
Fruquintinib is available as capsules containing 1 or 5 mg of the drug.1
Administer fruquintinib orally with or without food, at approximately the same time each day.1 Swallow fruquintinib capsules whole.1
If a dose of fruquintinib is missed, take the missed dose if <12 hours have elapsed; do not take 2 doses on the same day to make up for a missed dose.1
If vomiting occurs after taking a dose, do not administer an additional dose but continue with the next scheduled dose.1
Store fruquintinib capsules at 20-25°C (brief excursions permitted between 15-30°C).1
For the treatment of adults with metastatic colorectal cancer who have received prior treatment with fluoropyrimidine-, oxaliplatin-, and irinotecan-based chemotherapy; an anti-vascular endothelial growth factor (VEGF) therapy; and an anti-epidermal growth factor receptor (EGFR) therapy (if RAS wild-type and medically appropriate), the recommended dosage of fruquintinib is 5 mg orally once daily for the first 21 days of each 28-day cycle.1 Continue treatment until disease progression or unacceptable toxicity occurs.1
Dosage Modification for Toxicity
If adverse reactions occur during fruquintinib therapy, temporary interruption, dosage reduction, and/or permanent discontinuance of the drug may be necessary.1
If dosage modification is required, reduce the dosage of fruquintinib as described in Table 1.1 Permanently discontinue fruquintinib in patients who cannot tolerate a dosage of 3 mg orally once daily.1
Dosage Reduction Level | Recommended Dosage |
|---|---|
First dose reduction | 4 mg orally once daily |
Second dose reduction | 3 mg orally once daily |
Refer to Table 2 for recommended dosage modifications for fruquintinib based on adverse reaction.1
Adverse Reaction | Fruquintinib Dosage Modification Based on Severitya |
|---|---|
Hypertension | Grade 3: Temporarily withhold fruquintinib for grade 3 hypertension that persists despite antihypertensive therapy. Upon full resolution of hypertension or recovery to grade 1, resume fruquintinib at the next lower dosage level. Grade 4: Permanently discontinue fruquintinib. |
Hemorrhagic events | Grade 2: Temporarily withhold fruquintinib until full bleeding resolution or recovery to grade 1, then resume fruquintinib at the next lower dosage level. Grade 3 or 4: Permanently discontinue fruquintinib. |
Hepatotoxicity | ALT or AST >3 times upper limit of normal (ULN), or >3 times baseline if baseline was abnormal; or bilirubin >1.5 times ULN, or >1.5 times baseline if baseline was abnormal: Temporarily withhold fruquintinib and monitor AST/ALT and total bilirubin until total resolution to grade 1 or baseline, then resume fruquintinib at the next lower dosage level. ALT or AST >3 times ULN with concurrent total bilirubin >2 times ULN (without cholestasis or hemolysis): Permanently discontinue fruquintinib. AST or ALT >20 times ULN if baseline was normal, or >20 times baseline if baseline was abnormal; or bilirubin >10 times ULN if baseline was normal, or >10 times baseline if baseline was abnormal: Permanently discontinue fruquintinib. |
Proteinuria | Proteinuria ≥2 grams/24 hours: Temporarily withhold fruquintinib until proteinuria fully resolves or is <1 gram/24 hours. Upon recovery of proteinuria, resume fruquintinib at the next lower dosage level. Presence of nephrotic syndrome or if proteinuria does not recover to <1 gram/24 hours: Permanently discontinue fruquintinib. |
Palmar-plantar erythrodysesthesia (PPE) | Grade 2: Temporarily withhold fruquintinib and initiate supportive care. Upon full resolution of PPE or recovery to grade 1, resume fruquintinib at the same dosage level. Grade 3: Temporarily withhold fruquintinib and initiate supportive care. Upon full resolution of PPE or recovery to grade 1, resume fruquintinib at the next lower dosage level. |
Other adverse reactions | Grade 3: Temporarily withhold fruquintinib; upon full resolution of toxicity or recovery to grade 1, resume fruquintinib at the next lower dosage level. Grade 4: Discontinue fruquintinib. Consider resumption of fruquintinib at the next lower dosage level only if the toxicity is non-life threatening and fully resolves or recovers to grade 1 and the potential benefits of therapy outweigh the risks. |
aLevel of severity as defined by National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 5.0.1
No dosage adjustment of fruquintinib is necessary in patients with mild hepatic impairment (total bilirubin less than or equal to the upper limit of normal [ULN] with AST greater than ULN, or total bilirubin >1-1.5 times ULN and any AST).1
Fruquintinib has not been adequately studied in patients with moderate hepatic impairment (total bilirubin >1.5 times and <3 times ULN and any AST).1
Fruquintinib is not recommended for use in patients with severe hepatic impairment (total bilirubin >3 times ULN and any AST).1
The manufacturer makes no specific dosage recommendations in patients with renal impairment.1
The manufacturer makes no specific dosage recommendations for geriatric patients.1
Hypertension has been reported with fruquintinib.1 In clinical studies, hypertension occurred in 49% of patients with metastatic colorectal cancer (mCRC) receiving fruquintinib, including grade 3-4 events in 19% of patients.1 Hypertensive crisis was reported in 0.3% of patients.1 The onset of hypertension occurred a median of 14 days after the first dose of fruquintinib.1
Do not initiate fruquintinib unless there is adequate control of blood pressure (BP).1 Monitor BP on a weekly basis during the first month of fruquintinib therapy, then at least once monthly and as clinically indicated.1 Initiate or adjust antihypertensive therapy as needed.1 Withhold, reduce the dosage, or permanently discontinue fruquintinib based on the severity of hypertension.1
Serious hemorrhagic events, some fatal, have occurred in patients receiving fruquintinib.1 In clinical studies, GI hemorrhage was reported in 6% of patients who received fruquintinib, including 1% of patients who experienced a grade ≥3 event.1 Fatal hemorrhage occurred in 2 patients.1
Permanently discontinue fruquintinib if there is severe or life-threatening hemorrhage.1 Monitor the international normalized ratio (INR) in patients receiving anticoagulants.1
There is an increased risk for infection, including fatal infection, in patients receiving fruquintinib.1 In clinical studies, the incidence of infection was 18 and 12% in patients who received fruquintinib and placebo, respectively.1 Fatal infection also occurred more frequently in patients who received fruquintinib versus placebo (1% versus 0.3%, respectively).1
The most commonly reported infections in patients with mCRC who received fruquintinib were urinary tract infections (6.8%), upper respiratory tract infections (3.2%), and pneumonia (2.5%); fatal infections included pneumonia (0.4%), sepsis (0.2%), bacterial infection (0.1%), lower respiratory tract infection (0.1%), and septic shock (0.1%).1
Withhold fruquintinib if grade 3 or 4 infections occur, or if there is worsening infection of any grade.1 Upon resolution of the infection, resume fruquintinib at the same dosage.1
Gastrointestinal perforation has occurred in patients receiving fruquintinib.1 In clinical studies, 1.3% of patients with mCRC who received fruquintinib experienced a grade ≥3 GI perforation, including 1 fatal event.1
Permanently discontinue fruquintinib in patients who develop GI perforation or fistula.1
Liver injury can occur in patients receiving fruquintinib.1 In clinical studies, ALT or AST increases were reported in 48% of patients with mCRC who received fruquintinib, including grade ≥3 events in 5% of patients and fatal events in 0.2% of patients.1 The onset of liver enzyme elevations occurred a median of 29 days after the first dose of fruquintinib.1
Monitor liver function tests (ALT, AST, and bilirubin) before initiating fruquintinib and periodically during therapy.1 Temporarily withhold and then reduce the dosage or permanently discontinue fruquintinib based on the severity and persistence of hepatotoxicity.1
Proteinuria has been reported in patients receiving fruquintinib.1 In clinical studies, 36% of patients with mCRC who received fruquintinib developed proteinuria.1 Grade ≥3 events occurred in 2.5% of patients.1 The onset of proteinuria occurred a median of 22 days after the first dose of fruquintinib.1
Monitor for proteinuria before initiating fruquintinib and periodically during therapy.1 Withhold fruquintinib in patients with proteinuria ≥2 g/24 hours until improvement to grade 1 proteinuria or lower, then resume fruquintinib at a reduced dosage.1 Discontinue fruquintinib in patients who develop nephrotic syndrome.1
Palmar-plantar Erythrodysesthesia
Palmar-plantar erythrodyesthesia (PPE) has been reported in patients receiving fruquintinib.1 In clinical studies, PPE occurred in 35% of patients with mCRC who received fruquintinib, including grade 3 events in 8% of patients.1 The onset of PPE occurred a median of 19 days after the first dose of fruquintinib.1
Based on severity of PPE, withhold fruquintinib and then resume at the same or a reduced dosage.1
Posterior Reversible Encephalopathy Syndrome
Posterior reversible encephalopathy syndrome (PRES), a syndrome of subcortical vasogenic edema diagnosed by characteristic findings on MRI, has been reported in patients receiving fruquintinib.1 In clinical studies, 1 patient with mCRC who received fruquintinib developed PRES.1
Evaluate for PRES in any patient presenting with seizures, headache, visual disturbances, confusion, or altered mental function.1 Discontinue fruquintinib in patients who develop PRES.1
Patients who receive drugs that inhibit the vascular endothelial growth factor (VEGF) signaling pathway, such as fruquintinib, may have impaired wound healing.1 In clinical studies, 1 patient with mCRC who received fruquintinib developed a grade 2 event of wound dehiscence.1
Withhold fruquintinib for ≥2 weeks prior to major surgery.1
Withhold fruquintinib for ≥2 weeks after major surgery and until there is adequate wound healing.1 The safety of resuming fruquintinib after resolution of wound healing complications has not been established.1
There is a potential increased risk of arterial thromboembolic events in patients who receive fruquintinib.1 In clinical studies, 0.8% of patients with mCRC who received fruquintinib experienced an arterial thromboembolic event.1 The trials excluded patients with clinically important cardiovascular disease, uncontrolled hypertension, or prior thromboembolic events within the last 6 months.1
Carefully consider initiation of fruquintinib in patients with a recent history of thromboembolic events.1 Discontinue fruquintinib in patients who develop arterial thromboembolism.1
Allergic Reactions to FD&C Yellow No. 5 (Tartrazine) and No. 6 (Sunset Yellow FCF)
Fruquintinib 1 mg capsules contain FD&C Yellow No. 5 (tartrazine), which can lead to allergic-type reactions, including bronchial asthma, in susceptible patients.1 While the overall incidence of FD&C Yellow No. 5 (tartrazine) sensitivity in the general population is low, the sensitivity is more frequently observed in patients who also have aspirin hypersensitivity.1
Fruquintinib 1 mg also contains FD&C Yellow No. 6 (sunset yellow FCF), which can cause allergic reactions.1
Fetal/Neonatal Morbidity and Mortality
Based on animal data and the mechanism of action of fruquintinib, the drug may cause fetal harm when administered during pregnancy.1 In an embryo-fetal developmental study in pregnant rats, embryotoxic and teratogenic effects occurred at exposures below the clinical exposure.1
Verify pregnancy status in females of reproductive potential before initiating fruquintinib.1 Advise pregnant women of the potential fetal risk.1
Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment with fruquintinib and for 2 weeks after the last dose.1
Based on animal data and the mechanism of action of fruquintinib, the drug may cause fetal harm when administered during pregnancy.1
In an embryo-fetal developmental study in pregnant rats, oral administration of fruquintinib during organogenesis resulted in teratogenicity and embryo lethality at exposures below the clinical exposure.1 No data are available on the use of fruquintinib in pregnant women.1
Verify pregnancy status in females of reproductive potential prior to initiating fruquintinib.1 Advise pregnant women of the potential fetal risk.1
No data are available on the presence of fruquintinib or its metabolites in human milk.1 The effects of fruquintinib on the breast-fed child or on milk production are unknown.1
Due to the potential for serious adverse reactions in the breast-fed child, advise women to avoid breast-feeding while receiving fruquintinib and for 2 weeks following the last dose.1
Females and Males of Reproductive Potential
Verify pregnancy status in females of reproductive potential prior to initiation of fruquintinib.1
There are no data on the effects of the drug on human fertility.1 Based on animal studies, fruquintinib may impair female fertility (e.g., postimplantation loss).1
Advise females of reproductive potential and males with female partners of reproductive potential to use effective contraception during treatment with fruquintinib and for 2 weeks following the last dose.1
Safety and effectiveness of fruquintinib in pediatric patients <18 years of age have not been established.1
In the FRESCO-2 study, 46% of patients receiving fruquintinib were ≥65 years of age, which included 20% of patients ≥75 years of age.1 No overall differences in safety or effectiveness of fruquintinib were observed between geriatric and younger patients.1
In the FRESCO study, 18% of patients receiving fruquintinib were ≥65 years of age, and 1 patient was ≥75 years of age.1 No overall differences in safety or effectiveness of fruquintinib were observed between geriatric and younger patients.1
No clinically important differences in the pharmacokinetics of fruquintinib were observed in patients with mild hepatic impairment (total bilirubin less than or equal to the upper limit of normal [ULN] with AST greater than ULN, or total bilirubin >1-1.5 times ULN with any AST).1
Fruquintinib has not been adequately studied in patients with moderate hepatic impairment (total bilirubin >1.5 times and <3 times ULN and any AST).1 Fruquintinib is not recommended for use in patients with severe hepatic impairment (total bilirubin >3 times ULN and any AST).1 The effect of moderate to severe hepatic impairment on the pharmacokinetics of fruquintinib is unknown.1
No clinically important differences in the pharmacokinetics of fruquintinib were observed in patients with mild to moderate renal impairment (creatinine clearance 30-89 mL/minute).1
Adverse effects reported in ≥20% of patients receiving fruquintinib include hypertension, palmar-plantar erythrodysesthesia, proteinuria, dysphonia, abdominal pain, diarrhea, and asthenia.1
Fruquintinib is metabolized principally by cytochrome P-450 (CYP) isoenzyme 3A, and to a lesser extent by CYP2C8, CYP2C9, and CYP2C19.1 Fruquintinib also undergoes metabolism via non-CYP mediated routes (i.e., sulfation and glucuronidation).1
In vitro studies indicate that fruquintinib does not inhibit CYP1A2, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, or CYP3A, and does not induce CYP1A2, CYP2B6, or CYP3A.1
Fruquintinib is not a substrate of P-glycoprotein (P-gp), organic anion transporting polypeptide (OATP) 1B1, or OATP1B3.1 Fruquintinib does not inhibit OATP1B1, OATP1B3, organic anion transporter (OAT) 1, OAT3, organic cation transporter (OCT) 2, multidrug and toxin extrusion protein (MATE) 1, or MATE2-K.1
Drugs Affecting Hepatic Microsomal Enzymes
Concomitant use of fruquintinib with a strong CYP3A inducer may decrease the peak plasma concentration and AUC of fruquintinib, which may reduce the efficacy of fruquintinib.1
Concomitant use of fruquintinib with rifampin (a strong CYP3A inducer) decreased the peak plasma concentration and AUC of fruquintinib by 12 and 65%, respectively.1
Avoid concomitant use of fruquintinib with strong CYP3A inducers.1
Concomitant use of fruquintinib with a moderate CYP3A inducer may decrease the peak plasma concentration and AUC of fruquintinib, which may reduce the efficacy of fruquintinib.1
Concomitant use of fruquintinib with efavirenz (a moderate CYP3A inducer) is expected to decrease the peak plasma concentration and AUC of fruquintinib by 4 and 32%, respectively.1
If possible, avoid concomitant use of fruquintinib with moderate CYP3A inducers.1 If concomitant use cannot be avoided, continue to administer fruquintinib at the recommended dosage.1
Concomitant use of fruquintinib with dabigatran etexilate (a P-gp substrate) did not result in clinically important differences in the pharmacokinetics of dabigatran etexilate.1
No clinically important differences in fruquintinib pharmacokinetics were observed when used concomitantly with itraconazole (a strong CYP3A inhibitor).1
No clinically important differences in fruquintinib pharmacokinetics were observed when used concomitantly with the gastric-reducing agent rabeprazole (a proton pump inhibitor).1
Concomitant use of fruquintinib with rosuvastatin (a breast cancer resistance protein [BCRP] substrate) did not result in clinically important differences in the pharmacokinetics of rosuvastatin.1
Fruquintinib is a small molecule kinase inhibitor of vascular endothelial growth factor (VEGF) receptors 1, 2, and 3.1 In vitro, fruquintinib inhibits VEGF-mediated endothelial cell proliferation and tubular formation.1 In vitro and in vivo studies, fruquintinib inhibits VEGF-induced VEGFR-2 phosphorylation.1 In vivo, fruquintinib inhibits tumor growth in a colon cancer tumor xenograft mouse model.1
The exposure-response relationship of fruquintinib and the time course of pharmacodynamic response are unknown.1 Peak plasma concentrations and AUC of fruquintinib are dose-proportional over the dosage range of 1-6 mg.1 Following oral administration of fruquintinib, the median time to peak plasma concentration is approximately 2 hours.1 Steady-state concentrations of the drug are achieved after 14 days and the accumulation based on AUC is 4-fold.1 When fruquintinib was administered with a high-fat meal (800-1000 calories, 50% fat), there were no clinically important differences in the pharmacokinetics of the drug.1
Fruquintinib is approximately 95% bound to plasma proteins.1 Fruquintinib is metabolized principally via the cytochrome P-450 (CYP) pathway (by CYP3A, and to a lesser extent by CYP2C8, CYP2C9, and CYP2C19), and the non-CYP pathway (sulfation and glucuronidation).1 Following oral administration of a single radiolabeled 5 mg dose of fruquintinib, approximately 60% of the radioactivity was recovered in urine (0.5% as unchanged drug) and 30% in feces (5% as unchanged drug).1 The mean elimination half-life of fruquintinib is approximately 42 hours.1
Pharmacokinetics of fruquintinib are not significantly affected by age (18-82 years), sex, race (Asian, Black, and white), ethnicity (Hispanic/Latino versus non-Hispanic/Latino), body weight (48-108 kg), mild to severe renal impairment (creatinine clearance 15-89 mL/minute), and mild hepatic impairment (total bilirubin less than or equal to upper limit of normal [ULN] with AST greater than ULN, or total bilirubin >1-1.5 times ULN with any AST).1 The effect of moderate to severe hepatic impairment (total bilirubin >1.5 times ULN and any AST) on fruquintinib pharmacokinetics is unknown.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.
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.
Fruquintinib is obtained through designated specialty pharmacies.2 Visit the Fruzaqla® website ([Web]) for specific availability information.2
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Capsules | 1 mg | Fruzaqla® | Takeda Pharmaceuticals America |
5 mg | Fruzaqla® | Takeda Pharmaceuticals America |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions July 10, 2025. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, MD 20814.
Only references cited for selected revisions after 1984 are available electronically.
1. Takeda Pharmaceuticals America, Inc. Fruzaqla® (fruquintinib) ORAL prescribing information. 2025 Feb. [Web]
2. Dasari A, Lonardi S, Garcia-Carbonero R, et al. Fruquintinib versus placebo in patients with refractory metastatic colorectal cancer (FRESCO-2): an international, multicentre, randomised, double-blind, phase 3 study. Lancet . 2023; 402(10395):41-53.
3. Li J, Qin S, Xu RH, et al. Effect of Fruquintinib vs Placebo on Overall Survival in Patients With Previously Treated Metastatic Colorectal Cancer: The FRESCO Randomized Clinical Trial. JAMA . 2018; 319(24):2486-2496.
4. Ordering Fruzaqla®. From Takeda Pharmaceuticals website. Accessed 2024 Aug 29. [Web]
17. Chiorean EG, Nandakumar G, Fadelu T et al. Treatment of Patients With Late-Stage Colorectal Cancer: ASCO Resource-Stratified Guideline. JCO Glob Oncol . 2020; 6:414-438.
18. Morris VK, Kennedy EB, Baxter NN, et al. Treatment of Metastatic Colorectal Cancer: ASCO Guideline. J Clin Oncol . 2023;41(3):678-700.