Version July 2025
Dosage guidance:
Safety: Avoid initiation of vimseltinib in patients with active liver or biliary tract disease, increased serum transaminases, alkaline phosphatase, or total bilirubin or direct bilirubin > ULN at baseline.
Clinical considerations: During treatment with vimseltinib, assess kidney function utilizing alternative measures that are not based on serum creatinine.
Tenosynovial giant cell tumor, symptomatic: Oral: 30 mg twice weekly (ensure ≥72 hours between treatment doses); continue until disease progression or unacceptable toxicity (Ref).
Missed dose: If a dose is missed by ≤48 hours; administer the missed dose as soon as possible and resume the next dose on the regularly scheduled day. If a dose is missed by >48 hours, skip the missed dose, and administer the next dose on the regularly scheduled day. If a dose is vomited within 30 minutes of administration, repeat the dose; otherwise administer the next dose on the regularly scheduled day.
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
Kidney impairment prior to treatment initiation:
Note: Kidney function is calculated using the CKD-EPI equation; however, during treatment with vimseltinib, assess kidney function utilizing alternative measures that are not based on serum creatinine.
eGFR ≥30 mL/minute: There are no dosage adjustments provided in the manufacturer’s labeling; however, no clinically significant differences in vimseltinib pharmacokinetics were observed with mild to moderate kidney impairment.
eGFR <30 mL/minute: There are no dosage adjustments provided in the manufacturer’s labeling (effect on vimseltinib pharmacokinetics is unknown).
Hepatic impairment prior to treatment initiation:
Mild (total bilirubin ≤ ULN and AST > ULN or total bilirubin >1 to 1.5 × ULN and any AST) impairment: No dosage adjustment is necessary.
Moderate (total bilirubin >1.5 to 3 × ULN and any AST) or severe (total bilirubin >3 × ULN and any AST) impairment: There are no dosage adjustments provided in the manufacturer’s labeling (has not been studied).
Acute hepatotoxicity during treatment:
|
Dosage reduction levels |
Recommended vimseltinib dosage and schedule |
|---|---|
|
a Ensure a minimum of 72 hours between treatment doses. b If unable to tolerate 14 mg twice weekly, permanently discontinue vimseltinib. | |
|
Initial (usual) dosage |
30 mg twice weeklya |
|
First dosage reduction level |
20 mg twice weeklya |
|
Second dosage reduction level |
14 mg twice weeklya, b |
|
Severity |
Vimseltinib dosage modification |
|---|---|
|
AST and/or ALT >3 to 5 × ULN and total bilirubin elevations ≤2 × ULN OR Total bilirubin elevations ≤2 × ULN |
Withhold vimseltinib until AST and ALT resolve to ≤3 × ULN or baseline and total bilirubin resolves to baseline; resume vimseltinib at the next lower dose level (once drug induced liver injury has definitively been ruled out). Hepatotoxicity does not resolve within 4 weeks: Permanently discontinue vimseltinib. |
|
AST and/or ALT >3 to 5 × ULN and total bilirubin elevations >2 × ULN, or INR >1.5 and alkaline phosphatase <2 × ULN OR Total bilirubin elevations >2 × ULN |
Withhold vimseltinib until AST and ALT resolve to ≤3 × ULN or baseline and total bilirubin resolves to baseline; resume vimseltinib at the next lower dose level (once drug induced liver injury has definitively been ruled out). Hepatotoxicity does not resolve within 4 weeks: Permanently discontinue vimseltinib. |
|
AST and/or ALT >5 to 8 × ULN and total bilirubin ≤ ULN and without clinical symptoms |
Withhold vimseltinib until AST and ALT resolve to ≤3 × ULN or baseline. Although the manufacturer’s labeling does not provide guidance on resuming therapy once AST and ALT resolve to ≤3 × ULN or baseline, vimseltinib was resumed at the next lower dose level, if determined to be clinically appropriate, as part of the study protocol (Gelderblom 2024). Hepatotoxicity does not resolve within 4 weeks: Permanently discontinue vimseltinib. |
|
AST and/or ALT >5 to 8 × ULN and total bilirubin elevation > ULN, or INR >1.5, or alkaline phosphatase >2 × ULN |
Permanently discontinue vimseltinib. |
|
AST and/or ALT >8 × ULN |
Permanently discontinue vimseltinib. |
|
Dosage reduction levels |
Recommended vimseltinib dosage and schedule |
|---|---|
|
a Adverse reactions leading to dose interruptions or reductions during clinical trials included rash, periorbital edema, peripheral edema, fatigue, pruritus, facial edema, increased creatine phosphokinase (CPK), neuropathy, and hypertension b Ensure a minimum of 72 hours between treatment doses. c If unable to tolerate 14 mg twice weekly, permanently discontinue vimseltinib | |
|
Initial (usual) dosage |
30 mg twice weeklyb |
|
First dosage reduction level |
20 mg twice weeklyb |
|
Second dosage reduction level |
14 mg twice weeklyb,c |
Refer to adult dosing.
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified. Adverse reactions reported in adults.
>10%:
Cardiovascular: Hypertension (17%), peripheral edema (33%)
Dermatologic: Pruritus (29%), skin rash (47%)
Endocrine & metabolic: Decreased serum calcium (13%), hypercholesterolemia (43%), hypermagnesemia (13%)
Hematologic & oncologic: Decreased neutrophils (31%; grades 3/4: 1%), leukopenia (29%)
Hepatic: Increased serum alanine aminotransferase (24%), increased serum alkaline phosphatase (14%), increased serum aspartate aminotransferase (92%)
Hypersensitivity: Facial edema (31%)
Nervous system: Fatigue (59%), neuropathy (12%)
Ophthalmic: Increased lacrimation (12%), periorbital edema (60%)
Renal: Increased serum creatinine (17%)
1% to 10%:
Dermatologic: Cellulitis (1%)
Infection: Subcutaneous abscess (1%)
Ophthalmic: Blurred vision (6%), dry eye syndrome (10%)
Frequency not defined: Neuromuscular & skeletal: Increased creatine phosphokinase in blood specimen
There are no contraindications listed in the manufacturer's labeling.
Concerns related to adverse effects:
• Hepatotoxicity: Serious and fatal cases of liver injury have occurred with another CSF1R-targeted kinase inhibitor; vimseltinib has not been associated with serious and fatal liver injury. Treatment with vimseltinib resulted in elevations in AST and/or ALT, including grade 3 events, in a small percentage of patients. Higher vimseltinib exposure is associated with an increased risk of all grade elevations in AST and ALT. Advise patients to immediately report any signs/symptoms of severe liver injury.
• Serum creatinine elevations: In the clinical trial, a serum creatinine increase (compared to baseline) was observed; the maximum mean serum creatinine increase occurred by 10.4 weeks after treatment initiation. The observed increases in serum creatinine, which may be secondary to inhibition of renal tubular secretion transporters (OCT2 and MATE1), may not be associated with changes in kidney function and are reversible upon vimseltinib discontinuation.
Dosage form specific issues:
• Yellow dye: Vimseltinib 20 mg capsules contain FD&C Yellow No. 5 (tartrazine). Tartrazine may cause allergic reactions, including bronchial asthma; tartrazine sensitivity is frequently observed in patients who also have aspirin sensitivity. Vimseltinib 14 and 20 mg capsules contain FD&C Yellow No. 6 (Sunset Yellow FCF), which may also cause allergic reactions.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, Oral:
Romvimza: 14 mg [contains fd&c yellow #6 (sunset yellow)]
Romvimza: 20 mg [contains fd&c yellow #5 (tartrazine), fd&c yellow #6 (sunset yellow)]
Romvimza: 30 mg [contains fd&c blue #1 (brilliant blue)]
No
Capsules (Romvimza Oral)
14 mg (per each): $3,919.20
20 mg (per each): $3,919.20
30 mg (per each): $3,919.20
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.
Oral: Administer twice weekly on the same days each week (ensure ≥72 hours between treatment doses), with or without food. Swallow whole; do not open, break, or chew the capsules.
An FDA-approved patient medication guide, which is available with the product information and as follows, must be dispensed with this medication:
Romvimza: https://www.accessdata.fda.gov/drugsatfda_docs/label/2025/219304s000lbl.pdf#page=18
Tenosynovial giant cell tumor, symptomatic: Treatment (as a single agent) of symptomatic tenosynovial giant cell tumor (TGCT) in adults for which surgical resection will potentially cause worsening functional limitation or severe morbidity.
Substrate of P-glycoprotein (Minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential;
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.
BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors): Vimseltinib may increase serum concentration of BCRP/ABCG2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and BCRP substrates when possible. If combined, monitor for increased effects and toxicities of the BCRP substrate and consider dose adjustments. Risk D: Consider Therapy Modification
OCT2 Substrates (Clinically Relevant with Inhibitors): Vimseltinib may increase serum concentration of OCT2 Substrates (Clinically Relevant with Inhibitors). Management: Avoid concomitant use of vimseltinib and OCT2 substrates when possible. If combined, monitor for increased effects and toxicities of the OCT2 substrate and consider dose adjustments. Risk D: Consider Therapy Modification
P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors): Vimseltinib may increase serum concentration of P-glycoprotein/ABCB1 Substrates (High risk with Inhibitors). Management: Avoid concomitant use of vimseltinib and P-gp substrates when possible. If combined, administer vimseltinib at least 4 hours before the P-gp substrate. Risk D: Consider Therapy Modification
Verify pregnancy status prior to initiating treatment in patients who could become pregnant.
Patients who could become pregnant and patients with partners who could become pregnant should use effective contraception during therapy and for 1 month after the last dose of vimseltinib.
Adverse effects to fertility were observed in animal toxicology studies; data are lacking on possible fertility effects in humans.
Based on the mechanism of action and data from animal reproduction studies, in utero exposure to vimseltinib may cause fetal harm.
It is not known if vimseltinib is present in breast milk.
Due to the potential for serious adverse reactions in the breastfed infant, breastfeeding is not recommended by the manufacturer during therapy and for 1 month after the last dose of vimseltinib.
Monitor LFTs (AST, ALT, total bilirubin, direct bilirubin, alkaline phosphatase, and gamma-glutamyl transferase [GGT]) prior to treatment initiation, twice monthly for the first 2 months, then once every 3 months for the first year of therapy, and as clinically indicated thereafter. Verify pregnancy status prior to treatment initiation (in patients who could become pregnant). Monitor for signs/symptoms of hepatotoxicity. Monitor adherence.
Note: If assessing kidney function during vimseltinib treatment, utilize alternative measures that are not based on serum creatinine.
The American Society of Clinical Oncology hepatitis B virus (HBV) screening and management provisional clinical opinion (Ref) 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.
Vimseltinib is a potent and selective colony-stimulating factor 1 receptor (CSFR1)-targeted tyrosine kinase inhibitor (Ref). In vitro, vimseltinib inhibited autophosphorylation of CSF1R, receptor signaling induced by CSF1 ligand binding, and ultimately proliferation of CSFR1-expressing cells.
Distribution: Vd: 90 L.
Protein binding: 96.5% to human plasma proteins.
Metabolism: Primarily via oxidation, N-demethylation, and N-dealkylation; secondary biotransformation via N-demethylation, dehydrogenation, and oxidation pathways. CYP450 enzymes are not expected to have a major role in vimseltinib metabolism.
Half-life elimination: ~6 days.
Time to peak: 1 hour (range: 0.5 to 4 hours).
Excretion: Feces: ~43% (9.1% as unchanged drug); urine: 38% (5.1% as unchanged drug).
Clearance: 0.5 L/hour.
