Tovorafenib, a Type II rapidly accelerated fibrosarcoma (RAF) kinase inhibitor, is an antineoplastic agent.1
Tovorafenib is used for the treatment of relapsed or refractory pediatric low-grade glioma harboring a b-Raf serine-threonine kinase ( BRAF ) fusion or rearrangement, or BRAF V600 mutation, in patients ≥6 months of age.1 Tovorafenib has been designated an orphan drug by FDA for treatment of malignant glioma.2 The current indication for tovorafenib is approved under accelerated approval based on response rate and duration of response.1 Continued approval for this indication may be contingent upon verification and description of clinical benefit in a confirmatory trial(s).1
Efficacy of tovorafenib for the treatment of relapsed or refractory pediatric low-grade glioma harboring a BRAF fusion or rearrangement or BRAF V600 mutation was established in a phase 2, multicenter, open-label, single-arm trial (FIREFLY-1).1, 3 In FIREFLY-1, patients 6 months to 25 years of age with relapsed or refractory pediatric low-grade glioma with an activating BRAF alteration were treated with tovorafenib orally once weekly until disease progression or unacceptable toxicity.1, 3 Tovorafenib was administered at a dose of 420 mg/m2 (maximum 600 mg) based on body surface area (BSA), with doses ranging from 290 to 476 mg/m2 (0.76-1.25 times the approved recommended dosage).1 The major efficacy outcome was overall response rate, measured using the Response Assessment in Pediatric Neuro-Oncology (RAPNO) low-grade glioma criteria; additional outcomes included progression-free survival, duration of response, and time to response.3
A total of 76 patients were included in the efficacy population.1 The median age of these patients was 8.5 years; 53% were male and 53% were White.1 The study population consisted of patients who were previously treated with a median of 3 systemic regimens; 59% of the patients had previously received a mitogen-activated protein (MAP) kinase inhibitor.1 The most common BRAF alteration was a KIAA1549:BRAF fusion, which was present in 74% of patients at baseline.1 The overall response rate with tovorafenib was 51% (0% complete response, 37% partial response, and 14% minimal response).1, 3 The median duration of response was 13.8 months and time to response was 5.3 months among responders.1, 3 The median progression-free survival of the 76 patients in the study population was 13.8 months.3
Recurrent somatic alterations in BRAF , particularly V600E mutations and gene fusions, are encountered in certain CNS tumors in adults and children.204 These include select low- and high-grade gliomas in adults, such as pilocytic astrocytoma, pleomorphic xanthoastrocytoma (up to 70% with BRAF V600E), and ganglioglioma (20 to 60% with BRAF V600E), and pediatric low-grade gliomas.204 Surgery and/or radiation are the cornerstones of management of adult gliomas, with cytotoxic chemotherapy typically reserved for cases refractory to these interventions.204 In children, surgery is frequently utilized for diagnosis and symptomatic management, while cytotoxic chemotherapy is a typical mainstay of therapy for disease control due to long-term sequalae associated with radiotherapy.204
The 2022 European Association of Neuro-Oncology, European Network for Rare Cancers, and Society for Neuro-Oncology joint guidelines for management of circumscribed astrocytic gliomas, glioneuronal, and neuronal tumors make general recommendations for treatment of these conditions in adults and children.204 In patients with BRAF -altered pilocytic astrocytoma, pleomorphic xanthoastrocytoma, or ganglioglioma, these guidelines recommend that use of BRAF and/or mitogen-activated extracellular signal regulated kinase (MEK) inhibitors be considered.204
Tovorafenib is administered orally (as immediate-release tablets or oral suspension) with or without food.1
Administer at the same time once weekly.1 If a dose of tovorafenib is missed by ≤3 days, take the missed dose and resume dosing on the next regularly scheduled day.1 If a dose of tovorafenib is missed by >3 days, skip the missed dose and resume the regular dosing schedule.1 If vomiting occurs immediately after dose administration, repeat the dose.1
Store the tablets and oral suspension at 20—25ºC; excursions permitted to 15—30ºC.1
Reconstitute powder for oral suspension prior to use with 14 mL of room temperature water to yield a final concentration of 25 mg/mL of tovorafenib.1 If product foams after reconstitution, the deliverable volume is reduced.1
Each bottle delivers 300 mg of tovorafenib in 12 mL.1 For doses above 300 mg, reconstitute 2 bottles and split the dose as evenly as possible between the bottles (e.g., 6 mL and 7 mL for a 325 mg dose).1
Administer immediately after reconstitution using the supplied oral dosing syringe or via feeding tube (minimum 12-French).1 If not administered within 15 minutes after reconstitution, discard the solution.1
Swallow tablets whole with water.1 Do not chew, cut, or crush.1
The recommended dosage of tovorafenib in patients aged ≥6 months with relapsed or refractory low-grade glioma (with BRAF fusion or rearrangement or BRAF V600 mutation) and a body surface area (BSA) ≥0.3 m2, is 380 mg/m2 orally once weekly (maximum 600 mg once weekly) until disease progression or intolerable toxicity occurs.1 A recommended dosage of tovorafenib in pediatric patients with BSA <0.3 m2 has not been established.1 See Table 1 and Table 2 below for dosage recommendations based on BSA for the tablets or oral suspension.1
Body Surface Area (BSA) | Recommended Dosage |
|---|---|
0.3—0.89 m2 | Administer oral suspension (see Table 2) |
0.9—1.12 m2 | 400 mg once weekly |
1.13—1.39 m2 | 500 mg once weekly |
≥1.4 m2 | 600 mg once weekly |
BSA | Dose Volumea | Dosage |
|---|---|---|
0.3—0.35 m2 | 5 mL | 125 mg once weekly |
0.36—0.42 m2 | 6 mL | 150 mg once weekly |
0.43—0.48 m2 | 7 mL | 175 mg once weekly |
0.49—0.54 m2 | 8 mL | 200 mg once weekly |
0.55—0.63 m2 | 9 mL | 225 mg once weekly |
0.64—0.77 m2 | 11 mL | 275 mg once weekly |
0.78—0.83 m2 | 12 mL | 300 mg once weekly |
0.84—0.89 m2 | 14 mL | 350 mg once weekly |
0.9—1.05 m2 | 15 mL | 375 mg once weekly |
1.06—1.25 m2 | 18 mL | 450 mg once weekly |
1.26—1.39 m2 | 21 mL | 525 mg once weekly |
≥1.4 m2 | 24 mL | 600 mg once weekly |
aThe concentration of tovorafenib oral suspension is 25 mg/mL.1 Each bottle of suspension delivers 300 mg/12 mL.1
Dosage Modification for Toxicity
Dosage of tovorafenib may be reduced or therapy temporarily interrupted in patients who develop adverse effects.1 Recommended dosage reductions for tovorafenib tablets and oral suspension based on BSA are presented in Tables 3 and 4, respectively.1
BSA | First Dosage Reduction | Second Dosage Reduction |
|---|---|---|
0.3—1.12 m2 | Administer oral suspension once weekly (see Table 4) | Administer oral suspension once weekly (see Table 4) |
1.13—1.39 m2 | 400 mg once weekly | Administer oral suspension once weekly (see Table 4) |
≥1.4 m2 | 500 mg once weekly | 400 mg once weekly |
BSA | First Dosage Reduction | Second Dosage Reduction |
|---|---|---|
0.3—0.35 m2 | 100 mg once weekly | 75 mg once weekly |
0.36—0.42 m2 | 125 mg once weekly | 100 mg once weekly |
0.43—0.48 m2 | 150 mg once weekly | 125 mg once weekly |
0.49—0.54 m2 | 175 mg once weekly | 150 mg once weekly |
0.55—0.63 m2 | 200 mg once weekly | 150 mg once weekly |
0.64—0.77 m2 | 225 mg once weekly | 200 mg once weekly |
0.78—0.83 m2 | 250 mg once weekly | 200 mg once weekly |
0.84—0.89 m2 | 300 mg once weekly | 250 mg once weekly |
0.9—1.05 m2 | 325 mg once weekly | 275 mg once weekly |
1.06—1.25 m2 | 375 mg once weekly | 325 mg once weekly |
1.26—1.39 m2 | 450 mg once weekly | 375 mg once weekly |
≥1.4 m2 | 500 mg once weekly | 400 mg once weekly |
The recommended dosage modifications of tovorafenib for adverse reactions are described in Table 5.1
Adverse Drug Reaction (ADR) | Dosage Modification based on ADR Severitya |
|---|---|
Hemorrhage | Intolerable grade 2 or any grade 3 hemorrhage: Temporarily withhold tovorafenib; if hemorrhage improves to grade 0—1, resume at lower dosage. If hemorrhage is not improved, consider permanent discontinuation First occurrence of any grade 4 hemorrhage: Temporarily withhold tovorafenib; if hemorrhage improves to grade 0—1, resume at lower dosa alternatively, may permanently discontinue tovorafenib Recurrent grade 4 hemorrhage: Permanently discontinue tovorafenib |
Skin toxicity (including photosensitivity) | Intolerable grade 2 or grade 3—4 skin toxicity: Temporarily withhold tovorafenib; if skin toxicity improves to grade 0—1, resume at lower dosage. If skin toxicity is not improved, consider permanent discontinuation |
Hepatotoxicity | Grade 3 AST, ALT, or bilirubin: Temporarily withhold tovorafenib; if improvement to grade ≤2 or baseline within 8 days, resume therapy at the same dose. If abnormality does not resolve within 8 days, resume at the next lower dosage First occurrence of grade 4 hepatotoxicity: Temporarily withhold tovorafenib and if hepatotoxicity improves to grade 0—1, resume at lower dosa alternatively, may permanently discontinue Recurrent grade 4 hepatotoxicity: Permanently discontinue tovorafenib |
Other | Intolerable grade 2 or any grade 3: Temporarily withhold tovorafenib; if improvement to Grade 0—1, resume at lower dosage, if not improved, consider permanent discontinuation First occurrence of grade 4: Temporarily withhold tovorafenib; if improvement to grade 0—1, resume at lower dosa alternatively, may consider permanent discontinuation Recurrent grade 4: Permanently discontinue tovorafenib |
aNational Cancer Institute Common Terminology Criteria for Adverse Events (NCI CTCAE) version 5.0.1
The manufacturer states that no dosage adjustment is necessary in patients with mild (bilirubin ≤upper limit of normal [ULN] and AST >ULN, or bilirubin >1—1.5 times the ULN with any AST) hepatic impairment.1
Tovorafenib has not been studied in patients with moderate (bilirubin >1.5—3 times the ULN with any AST) to severe (bilirubin >3 times the ULN with any AST) hepatic impairment.1
The manufacturer states that no dosage adjustment is necessary in patients with mild to moderate renal impairment (estimated glomerular filtration rate [eGFR] ≥30 mL/minute/1.73 m2 based on Schwartz equation or Modification of Diet in Renal Disease [MDRD] equation).1
Tovorafenib has not been studied in patients with severe renal impairment (eGFR <30 mL/minute/1.73 m2).1
The manufacturer makes no specific dosage recommendations in geriatric patients.1
Hemorrhage, including major hemorrhage (e.g., symptomatic bleeding in a critical area or organ), has been reported with tovorafenib.1 Pooled safety data indicate hemorrhagic events occurred in 37% of patients, including epistaxis in 26% and intratumoral hemorrhage in 9%.1 Serious bleeding events developed in 5% of patients, including a grade 5 tumor hemorrhage, which occurred in 1 patient (0.6%).1 Hemorrhage resulting in permanent discontinuation of tovorafenib occurred in 2% of patients.1
Patients and caregivers should be advised of the risk of hemorrhage during tovorafenib therapy.1 Patients should be monitored for signs and symptoms of hemorrhage and evaluated as clinically necessary.1 Withhold and resume tovorafenib at a reduced dose upon improvement of symptoms, or permanently discontinue based on reaction severity.1
Skin Toxicity Including Photosensitivity
Rash, including maculopapular rash and photosensitivity, have been reported with tovorafenib.1 Pooled safety data indicate rash occurred in 67% of patients who received tovorafenib, which includes grade 3 rash in 12% of patients.1 In 15% of patients who developed rash, a dose interruption was needed, in 7% of patients, a dose reduction, and in 1% of patients, tovorafenib was permanently discontinued.1 Pooled safety data indicate dermatitis acneiform occurred in 26% of patients who received tovorafenib, which includes grade 3 dermatitis acneiform in 0.6% of patients.1 In 2% of patients who developed dermatitis acneiform, dose reduction was required.1 Patients should be monitored for new or worsening skin reactions.1 Consider dermatologic consultation and initiate supportive care as clinically necessary.1 Withhold, dose reduce, or permanently discontinue tovorafenib based on adverse reaction severity.1
Pooled safety data indicate photosensitivity occurred in 12% of patients who received tovorafenib, which includes grade 3 events, occurring in 0.6% of patients.1 Patients should use precautionary measures against ultraviolet exposure (e.g., sunscreen, sunglasses, and/or protective clothing) during treatment with tovorafenib.1 Withhold, dose reduce, or permanently discontinue tovorafenib based on adverse reaction severity.1
Hepatotoxicity has been reported with tovorafenib.1 Pooled safety data indicate that increases in ALT and AST occurred in 42% and 74% of patients, respectively, including grade 3 ALT in 4% and increased AST in 2% of patients.1 The median time to onset was 14 days (range, 3 to 280 days).1 In 5% of patients, increases in ALT or AST necessitated dosage interruptions.1 Dose reductions were required in 1.2% of patients.1 Bilirubin increases occurred in 23% of patients, which includes grade 3 increases in 0.6% of patients.1 One adult patient with an advanced non-CNS solid tumor developed hyperbilirubinemia, leading to treatment discontinuation.1
Evaluate liver function tests (e.g., ALT, AST, bilirubin) prior to initiation, 1 month after initiation, and then every 3 months thereafter and as clinically indicated.1 Withhold tovorafenib and resume at the same or reduced dose upon improvement, or permanently discontinue based on severity.1
Reductions in growth velocity have occurred with tovorafenib.1 In the FIREFLY-1 trial, adverse growth effects occurred in 15% of patients ≤18 years of a this includes grade 3 events that occurred in 5% of patients.1 Permanent discontinuation of therapy due to reductions in growth velocity occurred in 2% of patients (n=2).1 Growth velocity recovered after interrupting tovorafenib treatment.1 Routinely monitor growth during tovorafenib treatment.1
Fetal/Neonatal Morbidity and Mortality
Based on animal data and its mechanism of action, tovorafenib may cause fetal harm when administered during pregnancy.1 Embryolethality was detected in rats at doses approximately 0.8-fold the human exposure at the recommended dose based on AUC.1 Verify pregnancy status in females of reproductive potential before treatment initiation.1 Advise pregnant women and females of reproductive potential of the potential fetal risk.1 Advise females of reproductive potential to use effective non-hormonal contraception during tovorafenib therapy and for 28 days following the final dose, as some hormonal contraceptives may not be effective during treatment.1 Advise male patients with female partners of reproductive potential to use effective nonhormonal contraception during tovorafenib therapy and for 2 weeks following the final dose.1
Neurofibromatosis Type 1 Associated Tumors
Nonclinical data in neurofibromatosis type 1 (NF1) models without BRAF alterations indicate that tovorafenib may promote tumor growth in NF1 tumors.1 Confirm evidence of a BRAF alteration prior to initiation.1
No data are available on tovorafenib use in pregnant women.1 Based on animal data and its mechanism of action, tovorafenib may cause fetal harm when administered during pregnancy.1 Embryolethality was detected in rats at doses approximately 0.8-fold the human exposure at the recommended dose based on AUC.1 Pregnant women should be informed of the potential fetal risk with tovorafenib.1
No data are available on the presence of tovorafenib or its metabolites in human milk.1 The effects of the drug on the breast-fed child or on milk production are not known.1 Due to the potential for serious adverse reactions in a breast-fed child from tovorafenib, advise lactating women not to breast-feed while receiving tovorafenib therapy and for 2 weeks following the final dose.1
Females and Males of Reproductive Potential
May cause fetal harm when administered during pregnancy.1 Prior to initiation of tovorafenib, verify pregnancy status in females of reproductive potential.1
Advise females of reproductive potential to use effective non-hormonal contraception during tovorafenib therapy and for 28 days following the final dose, as some hormonal contraceptives may not be effective during treatment.1
Advise male patients with female partners of reproductive potential to use effective nonhormonal contraception during tovorafenib therapy and for 2 weeks following the final dose.1
Animal data indicate that tovorafenib may impact fertility.1 The effects on male fertility were reversible; however, the effects on female fertility were irreversible.1
Safety and efficacy of tovorafenib in pediatric patients aged ≥6 months with relapsed or refractory pediatric low-grade glioma harboring a BRAF fusion or rearrangement, or BRAF V600 mutation are established based on data from a multicenter, open-label, single-arm clinical trial.1
The effectiveness of tovorafenib was evaluated in 76 pediatric patients with relapsed or refractory low-grade glioma.1 The safety of tovorafenib was evaluated in 137 patients from arms 1 and 2 in the FIREFLY-1 study.1 Of the 137 patients with relapsed or refractory low-grade glioma in the FIREFLY-1 study, 2% (n=3) were 6 months to <2 years of age, 67% (n=92) were 2 to <12 years of age, and 31% (n=42) were >12 years of age.1 Peak plasma concentrations and total exposure to tovorafenib based on AUC in pediatric patients aged 11 months to 17 years were within the range observed in adults using the same dosage based on BSA.1
Safety and efficacy of tovorafenib in patients aged <6 months have not been established.1
Reductions from baseline in Z-scores compared to normal values for age and sex were observed in patients with low-grade glioma treated with tovorafenib for up to 24 months.1 No evidence of premature closure of epiphyseal growth plates or advancement of bone age were observed in hand radiographs of the 19 patients with reduced growth velocity.1 Following treatment interruption, there was an observed recovery in growth and an increase in Z-scores.1 Growth should be monitored on a routine basis during treatment.1
No clinically significant differences in tovorafenib pharmacokinetics were observed based on age (range, 1—94 years).1
No clinically significant differences in tovorafenib pharmacokinetics have been observed in patients with mild (bilirubin ≤upper limit of normal [ULN] and AST >ULN or bilirubin >1—1.5 times ULN and any AST) hepatic impairment.1 Tovorafenib has not been studied in patients with moderate (bilirubin >1.5—3 times ULN and any AST) to severe (bilirubin >3 times ULN and any AST) hepatic impairment.1
No clinically significant differences in tovorafenib pharmacokinetics have been observed in patients with mild-to-moderate renal impairment (estimated glomerular filtration rate [eGFR] ≥30 mL/min per 1.73 m2 calculated by Schwartz equation or Modification of Diet in Renal Disease [MDRD] equation).1 Tovorafenib has not been studied in patients with severe renal impairment (eGFR <30 mL/min per 1.73 m2).1
Adverse effects reported in at least 30% of patients receiving tovorafenib include rash, hair color changes, fatigue, viral infection, vomiting, headache, hemorrhage, pyrexia, dry skin, constipation, nausea, dermatitis acneiform, and upper respiratory tract infection.1
In vitro, tovorafenib is metabolized principally by aldehyde oxidase and cytochrome P450 (CYP) isoenzyme 2C8, and undergoes minimal metabolism by CYP3A, CYP2C9, and CYP2C19.1 In vitro, tovorafenib is both an inhibitor and inducer of CYP3A, CYP2C8, CYP2C9, and CYP2C19.1 Tovorafenib is an inducer of CYP1A2 and CYP2B6, but does not inhibit CYP1A2, CYP2B6, or CYP2D6 at clinically relevant concentrations.1
Tovorafenib inhibits breast cancer resistance protein (BCRP) at clinically relevant concentrations, but is not a substrate of BCRP, P-glycoprotein (P-gp), organic anion transporter polypeptide (OATP) 1B1, or OATP1B3.1 It has not been evaluated if tovorafenib is a substrate of organic anion transporter (OAT) 1, OAT3, multidrug and toxin extrusion (MATE) 1, MATE2-K, or organic cation transporter (OCT)2.1
Drugs Affecting Hepatic Microsomal Enzymes
Moderate and Strong CYP2C8 Inhibitors
Concomitant use of tovorafenib (a CYP2C8 substrate), with a moderate or potent CYP2C8 inhibitor is predicted to increase tovorafenib exposure, thereby increasing the risk of adverse effects from tovorafenib.1 Concomitant use of tovorafenib and moderate or strong CYP2C8 inhibitors should be avoided.1
Moderate and Strong CYP2C8 Inducers
Concomitant use of tovorafenib (a CYP2C8 substrate), with a moderate or strong CYP2C8 inducer is predicted to decrease tovorafenib exposure, potentially reducing its efficacy.1 Concomitant use of tovorafenib and moderate or strong CYP2C8 inducers should be avoided.1
Drugs Metabolized by Hepatic Microsomal Enzymes
Tovorafenib is predicted to decrease the exposure of certain CYP3A substrates.1 Avoid concomitant use of tovorafenib with certain CYP3A substates where minimal concentration changes could result in loss of therapeutic efficacy.1 If concomitant use of tovorafenib with the CYP3A substrate cannot be avoided, monitor patients for loss of therapeutic efficacy unless otherwise indicated in the substrate prescribing information.1
Concomitant use of tovorafenib with midazolam (a CYP3A4 substrate) is predicted to decrease peak plasma concentrations and exposure (based on AUC) of midazolam by at least 20%.1
Concomitant use of tovorafenib with hormonal contraceptives (a CYP3A substrate) may decrease exposure to progestin and ethinyl estradiol, resulting in contraceptive failure and/or breakthrough bleeding.1 Avoid concomitant use of tovorafenib with hormonal contraceptives.1 If concomitant use cannot be avoided, use an additional non-hormonal method of contraception during treatment and for 28 days following the final dose of tovorafenib.1
Tovorafenib is a Type II rapidly accelerated fibrosarcoma (RAF) kinase inhibitor of mutant b-Raf serine-threonine kinase ( BRAF ) V600E, wild-type BRAF , and wild-type c-RAF serine-threonine kinase ( CRAF ) kinases.1 The drug exhibits antitumor activity in cultured cells and xenograft tumor models harboring BRAF V600E and V600D mutations.1 Tovorafenib also demonstrates antitumor activity in a xenograft tumor model harboring BRAF fusion.1
Following a single oral dose of tovorafenib tablets or suspension, peak plasma concentrations are achieved after a median of 3 hours (range, 1.5—4 hours).1 Following once weekly dosing of tovorafenib, steady state is attained after 12 days.1 Exposure to tovorafenib increases in a dose proportional manner, with no clinically significant accumulation of tovorafenib at recommended doses.1 Higher exposure to tovorafenib is associated with an increased risk of skin rash, elevations in liver enzymes, and elevations in creatine phosphokinase.1 Administration of tovorafenib tablets with a high-fat meal does not alter total exposure or peak plasma concentrations of tovorafenib, but delays time to peak plasma concentrations to 6.5 hours.1 In vitro, tovorafenib is 97.5% bound to human plasma proteins.1 Tovorafenib is metabolized principally by aldehyde oxidase and cytochrome P450 (CYP) 2C8 in vitro, and to a lesser extent by CYP3A, CYP2C9, and CYP2C19.1 Following oral administration of a single radiolabeled dose of tovorafenib, 65% of the total radiolabeled dose was recovered in the feces (8.6% of the dose as unchanged drug), and 27% was recovered in urine (0.2% of the dose as unchanged drug).1 The mean elimination half-life of tovorafenib is 56 hours.1 The pharmacokinetics of tovorafenib are not affected by age (1—94 years), sex, race (White, Black, Asian), mild hepatic impairment (bilirubin ≤upper limit of normal [ULN] and AST >ULN or bilirubin >1—1.5 times ULN and any AST), and mild to moderate renal impairment (estimated glomerular filtration rate [eGFR] ≥30 mL/min per 1.73 m2 calculated by Schwartz equation or Modification of Diet in Renal Disease [MDRD] equation).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.
Tovorafenib is available only from a designated specialty pharmacy.4 The manufacturer should be contacted for additional information.4
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | For oral suspension | 25 mg/mL | Ojemda® | Day One Biopharmaceuticals |
Tablets, film-coated | 100 mg | Ojemda® | Day One Biopharmaceuticals |
AHFS® Drug Information. © Copyright, 1959-2026, Selected Revisions December 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. Day One Biopharmaceuticals, Inc. OJEMDA® (tovorafenib) prescribing information. 2024 June. [Web]
2. US Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. Accessed 2024 Aug 15. [Web]
3. Kilburn LB, Khuong-Quang DA, Hansford JR, et al. The type II RAF inhibitor tovorafenib in relapsed/refractory pediatric low-grade glioma: the phase 2 FIREFLY-1 trial [published correction appears in Nat Med. 2024 May;30(5):1500. doi: 10.1038/s41591-024-02910-1]. Nat Med . 2024; 30(1):207-217
4. EveryDay Support. From Day One Biopharmaceuticals website. Accessed 2024 Aug 16. [Web]
204. Rudà R, Capper D, Waldman AD et al. EANO-EURACAN-SNO guidelines on circumscribed astrocytic gliomas, glioneuronal, and neuronal tumors. Neuro Oncol . 2022; 24:2015-2034.