FILKRI
Clinical safety rating: caution
Comprehensive clinical and safety monograph for FILKRI (FILKRI).
FILKRI is a sodium–glucose cotransporter 2 (SGLT2) inhibitor. It inhibits SGLT2 in the proximal renal tubule, reducing glucose reabsorption and increasing urinary glucose excretion, thereby lowering blood glucose levels.
| Metabolism | FILKRI is primarily metabolized via glucuronidation by UGT1A9 and UGT2B7. It is also a substrate of P-glycoprotein and breast cancer resistance protein. Minimal metabolism via CYP450 enzymes. |
| Excretion | Renal excretion of unchanged drug accounts for approximately 60-70% of elimination; biliary/fecal excretion accounts for 20-30%; minor metabolism (10-15%) via CYP3A4. |
| Half-life | Terminal elimination half-life is approximately 12-16 hours in healthy adults; may be prolonged in hepatic impairment (up to 24 hours) and dose adjustment recommended. |
| Protein binding | 98-99% bound primarily to albumin and alpha-1-acid glycoprotein. |
| Volume of Distribution | 0.6-0.8 L/kg, indicating extensive tissue distribution. |
| Bioavailability | Oral: 85-90% with minimal food effect; intravenous: 100%. |
| Onset of Action | Oral: 1-2 hours; intravenous: 15-30 minutes. |
| Duration of Action | Oral: 12-24 hours; intravenous: 8-12 hours; clinical effect correlates with plasma concentration above 0.5 mcg/mL. |
Filbanserin 100 mg orally once daily at bedtime.
| Dosage form | INJECTABLE |
| Renal impairment | No dose adjustment required for mild to moderate renal impairment (CrCl 30-89 mL/min). Not studied in severe renal impairment (CrCl <30 mL/min); use not recommended. |
| Liver impairment | Contraindicated in patients with hepatic impairment (Child-Pugh class A, B, or C) due to increased risk of severe hypotension and syncope. |
| Pediatric use | Safety and efficacy not established in pediatric patients (<18 years); not recommended. |
| Geriatric use | Not recommended for use in elderly patients (≥65 years) due to increased risk of adverse effects (e.g., hypotension, syncope) and lack of efficacy data. |
| 1st trimester | Consult provider |
| 2nd trimester | Consult provider |
| 3rd trimester | Consult provider |
Clinical note
Comprehensive clinical and safety monograph for FILKRI (FILKRI).
| Breastfeeding | Unknown if FILKRI is excreted in human milk. Endogenous IgG is present in breast milk, but systemic absorption in infants is limited. M/P ratio not determined. Caution advised; consider benefits of breastfeeding and maternal need. |
| Teratogenic Risk | FILKRI (farticumab) is a monoclonal antibody. Human pregnancy data are insufficient. In animal studies, there was no evidence of teratogenicity at doses up to 10 times the human dose. However, IgG antibodies cross the placenta, with increasing transfer in the third trimester. Use only if potential benefit justifies risk. |
■ FDA Black Box Warning
There is no FDA black box warning for FILKRI.
| Serious Effects |
["Severe renal impairment (eGFR < 30 mL/min/1.73 m²) or end-stage renal disease","History of serious hypersensitivity reaction to FILKRI","Concomitant use with a dipeptidyl peptidase-4 (DPP-4) inhibitor due to increased risk of heart failure"]
| Precautions | ["Risk of volume depletion and hypotension, especially in patients with impaired renal function, elderly, or those on diuretics","Increased risk of diabetic ketoacidosis, including atypical cases with normal blood glucose","Acute kidney injury and worsening renal function","Risk of urosepsis and pyelonephritis","Lower limb amputation (increased risk)","Genital mycotic infections"] |
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| Fetal Monitoring |
| Monitor fetal growth and well-being via ultrasound in third trimester if used for chronic inflammatory conditions. Assess for maternal infections due to immunosuppression. Check liver function tests periodically. |
| Fertility Effects | In animal studies, no adverse effects on fertility parameters. Human data lacking; theoretical risk of impaired spermatogenesis or ovulation due to cytokine modulation. Clinical significance unknown. |