Vumerity (diroximel fumarate)
Multiple Sclerosis Agents, General Oral Capsule,Delayed Release (Enteric Coated)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Diroximel fumarate, a fumaric acid derivative, has immunomodulatory and disease-modifying activity in multiple sclerosis (MS). Diroximel fumarate is metabolized to the same active metabolite (monomethyl fumarate (MMF)) as dimethyl fumarate.
Diroximel fumarate is a fumaric acid derivative; the drug is an aminoethyl ester of monomethyl fumarate (MMF). MMF has immunomodulatory and disease-modifying activity in multiple sclerosis (MS). The exact mechanism by which diroximel fumarate exerts its therapeutic effect in MS is unknown.
MMF, the active metabolite of diroximel fumarate, has been shown to activate the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway in vitro and in vivo in animals and humans. The Nrf2 pathway is involved in the cellular response to oxidative stress. In vitro and animal studies suggest that Nrf2-dependent upregulation of antioxidant response genes by MMF may protect various cells and tissues, including some in the CNS, from experimental toxic oxidative stress.
Activation of the Nrf2 pathway by fumaric acid derivatives also may inhibit proliferation of lymphocytes and hematopoietic stem cells. While fumaric acid derivative therapy causes substantial, dose-dependent reductions in peripheral lymphocytes, subsets of lymphocytes appear to be affected differently. In particular, more pronounced reductions in CD8+ T-cell counts compared with CD4+ T-cell counts have been observed; subsets of other lymphocytes (e.g., memory T-cells, B-cells, natural killer (NK) cells) also have been altered.
Such alterations in the composition of peripheral lymphocytes are thought to shift the immune profile towards an anti-inflammatory state in patients with MS.
In addition, MMF has been shown to be a nicotinic acid receptor agonist in vitro. Nicotinic acid and fumaric acid derivatives can cause skin flushing as an adverse reaction; it has been suggested that such flushing reactions may be mediated by the activation of hydroxy-carboxylic acid receptor 2 (HCA2) and involve the formation of prostaglandins.
Following oral administration of diroximel fumarate delayed-release capsules, the drug is rapidly and extensively metabolized by esterases, which are present in the GI tract, blood, and tissues, to the active MMF metabolite before it reaches the systemic circulation; because plasma concentrations of the parent drug are not quantifiable after oral administration, all pharmacokinetic analyses have been performed with plasma MMF concentrations. Peak plasma concentration and systemic exposure of MMF increase in a dose-proportional manner over a diroximel fumarate dose range of 462-924 mg; accumulation of MMF does not occur following multiple doses of diroximel fumarate. When administered orally, 462 mg of diroximel fumarate and 240 mg of dimethyl fumarate produce bioequivalent exposure to MMF.
Following oral administration of diroximel fumarate delayed-release capsules, the median time to peak plasma MMF concentrations is 2.5-3 hours. Administration of diroximel fumarate delayed-release capsule with a high-fat, high-calorie meal (900-1000 calories, 50% of calories from fat) reduces peak plasma MMF concentrations by approximately 44% and delays time to peak plasma concentration from 2.5 hours to 7 hours compared with administration in a fasted state. Administration of the drug with a medium-fat, medium-calorie (650-700 calories, 25-30 g fat) or low-fat, low-calorie meal (350-400 calories, 10-15 g fat) reduces peak plasma MMF concentrations by approximately 25 or 12%, respectively, and delays time to peak plasma concentration from 2.5 hours to 4.5 hours compared with administration in a fasted state.
Administration of diroximel fumarate with food (regardless of the fat content) did not affect systemic exposure of MMF. MMF is 27-45% bound to plasma proteins independent of concentration. MMF distributes into the CNS.
Diroximel fumarate is extensively metabolized to MMF by esterases present in the GI tract, blood, and tissues before it reaches the systemic circulation. MMF is also metabolized via the tricarboxylic acid (TCA) cycle, with no involvement of cytochrome P450 (CYP) pathways. Fumaric acid, citric acid, and glucose are the major metabolites of MMF in plasma.
Esterase metabolism of diroximel fumarate also produces 2-hydroxyethyl succinimide (HES), an inactive major metabolite. MMF is primarily expired as carbon dioxide with less than 0.3% of the dose recovered in urine. HES is primarily eliminated in urine (58-63% of the dose).
The terminal half-life of MMF is approximately 1 hour.
The pharmacokinetics of MMF following administration of diroximel fumarate are not affected by age (18-79 years), sex, or race.
USES: Diroximel fumarate is used to treat multiple sclerosis (MS). It is not a cure for MS. It helps decrease the number of episodes of worsening MS.
Generic name: diroximel fumarate
Pronunciation: (dye-ROX-i-mel FUE-ma-rate)
Drug class: Multiple Sclerosis Agents, General
Therapeutic class: Multiple Sclerosis Agents
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Vumerity
Indications
The following indications are listed for Vumerity:
- Relapsing Form Of Multiple Sclerosis
- Secondary Progressive Multiple Sclerosis
Also known as: Multiple Sclerosis, Relapsing Form.
Dosing
The recommended initial dosage of diroximel fumarate in adults with relapsing forms of multiple sclerosis (MS) is 231 mg twice daily. After 7 days, the dosage should be increased to a maintenance dosage of 462 mg twice daily.
In patients not tolerating a dosage of 462 mg twice daily, consider a temporary reduction to 231 mg twice daily; however, the recommended maintenance dosage of 462 mg twice daily should be resumed within 4 weeks. Consider discontinuance of the drug in patients unable to tolerate a maintenance dosage of 462 mg twice daily.
Dosage adjustment is not required in patients with hepatic impairment. Although no studies have been conducted, hepatic impairment is not expected to affect systemic exposure to the active metabolite of diroximel fumarate.
Dosage adjustment is not required in patients with mild renal impairment. Because of an increase in exposure to a major metabolite, diroximel fumarate is not recommended in patients with moderate or severe renal impairment.
Administer diroximel fumarate delayed-release capsules orally twice daily with or without food. Swallow capsules whole and intact; do not crush, chew, or open capsule contents and sprinkle on food.
The incidence of flushing may be reduced if the drug is taken with food; however, avoid administration with a high-fat, high-calorie meal or snack. The meal or snack should contain no more than 700 calories and no more than 30 g fat.
| Drug label | Dosing type | Instructions |
|---|---|---|
| Vumerity Dr 231 Mg Capsule | Maintenance | Take 2 capsules (462 mg) by oral route 2 times per day. |
No dosing information is available for this tab.
Drug interactions
Diroximel fumarate is not metabolized by cytochrome P-450 (CYP) isoenzymes; therefore, clinically important interactions with CYP inhibitors or inducers are not expected. Studies involving inhibition or induction of CYP isoenzymes, P-glycoprotein (P-gp), or protein binding have not revealed any potential drug interactions for diroximel fumarate or its active metabolite, monomethyl fumarate (MMF).
Diroximel fumarate and its metabolites did not inhibit CYP isoenzymes 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, or 3A4/5 or induce CYP isoenzymes 1A2, 2B6, or 3A4/5 in vitro. The drug did not inhibit P-gp in vivo. The major circulating inactive metabolite 2-hydroxyethyl succinimide (HES) did not inhibit P-gp and was neither a substrate nor an inhibitor of breast cancer resistance protein (BCRP), multidrug and toxin extrusion transporter (MATE) 1, MATE2K, organic anion transporter (OAT) 1, OAT3, or organic cation transporter (OCT) 2.
Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
Immunosuppressives; Immunomodulators/Efalizumab; Natalizumab
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: Natalizumab,(1-3) efalizumab,(4) immunosuppressives, and immunomodulators all suppress the immune system.
CLINICAL EFFECTS: Concurrent use of natalizumab(1-3) or efalizumab(4) with immunosuppressives or immunomodulators may result in an increased risk of infections, including progressive multifocal leukoencephalopathy (PML), an opportunistic infection caused by the JC virus (JCV).
PREDISPOSING FACTORS: Previous JCV infection, longer duration of natalizumab treatment - especially if greater than 2 years, and prior or concomitant treatment with immunosuppressant medication are all independent risk factors which increase the risk for PML.(1,5) The FDA has estimated PML incidence stratified by risk factors: If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment less than 25 months, incidence <1/1,000. If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment less than 25 months, incidence 2/1,000 If anti-JCV antibody positive, no prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 4/1,000 If anti-JCV antibody positive, history of prior immunosuppressant use and natalizumab treatment 25-48 months, incidence 11/1,000.
PATIENT MANAGEMENT: The US manufacturer of natalizumab states patients with Crohn's disease should not receive concurrent immunosuppressants, with the exception of limited overlap of corticosteroids, due to the increased risk for PML. For new natalizumab patients currently receiving chronic oral corticosteroids for Crohn's Disease, begin corticosteroid taper when therapeutic response to natalizumab has occurred. If corticosteroids cannot be discontinued within six months of starting natalizumab, discontinue natalizumab.(3) The US manufacturer of natalizumab states that natalizumab should not ordinarily be used in multiple sclerosis patients receiving immunosuppressants or immunomodulators due to the increased risk for PML. Immunosuppressives include, but are not limited to azathioprine, cyclophosphamide, cyclosporine, mercaptopurine, methotrexate, mitoxantrone, mycophenolate, and corticosteroids.(3,6) The UK manufacturer of natalizumab states that concurrent use with immunosuppressives or antineoplastic agents is contraindicated.(1) The Canadian manufacturer of natalizumab states that natalizumab should not be used with immunosuppressive or immunomodulatory agents.(2) The US manufacturer of certolizumab states that concurrent therapy with natalizumab is not recommended.(7)
DISCUSSION: Progressive multifocal leukoencephalopathy has been reported in patients receiving concurrent natalizumab were recently or concomitantly taking immunomodulators or immunosuppressants.(1-5,8,9) In a retrospective cohort study of multiple sclerosis patients newly initiated on a disease-modifying therapy, use of high-efficacy agents (alemtuzumab, natalizumab, or ocrelizumab) resulted in the same risk of overall infections as moderate-efficacy agents, but there was an elevated risk of serious infections (adjusted hazard ratio [aHR] = 1.24, 95% confidence interval (CI) = 1.06-1.44) and UTIs (aHR = 1.21, 95% CI = 1.14-1.30).(10)
Selected Immunosuppressants/Nadofaragene Firadenovec
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: Nadofaragene firadenovec may contain low levels of replication-competent adenovirus.(1)
CLINICAL EFFECTS: Concurrent use of nadofaragene firadenovec in patients receiving immunosuppressive therapy may cause disseminated adenovirus infection.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Individuals who are immunosuppressed or immune-deficient should not receive nadofaragene firadenovec.(1)
DISCUSSION: Nadofaragene firadenovec is a non-replicating adenoviral vector-based gene therapy but may contain low levels of replication-competent adenovirus. Immunocompromised persons, including those receiving immunosuppressant therapy, may be at risk for disseminated adenovirus infection.(1)
Selected Immunosuppressants/Talimogene Laherparepvec
SEVERITY LEVEL: 1-Contraindicated Drug Combination: This drug combination is contraindicated and generally should not be dispensed or administered to the same patient.
MECHANISM OF ACTION: Talimogene laherparepvec is a live, attenuated herpes simplex virus.(1)
CLINICAL EFFECTS: Concurrent use of talimogene laherparepvec in patients receiving immunosuppressive therapy may cause a life-threatening disseminated herpetic infection.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Talimogene laherparepvec is contraindicated in immunosuppressed patients.(1) The magnitude of immunocompromise and associated risks due to immunosuppressant drugs should be determined by a physician.
DISCUSSION: Concurrent use of talimogene laherparepvec in patients receiving immunosuppressive therapy may cause a life-threatening disseminated herpetic infection.(1)
Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
Immunosuppressives; Immunomodulators/Baricitinib
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Concurrent use of baricitinib with other biologic disease-modifying antirheumatic drugs (DMARDs) or potent immunosuppressants such as azathioprine or cyclosporine may result in additive or synergistic effects on the immune system.
CLINICAL EFFECTS: Concurrent use of baricitinib with other biologic DMARDs or potent immunosuppressants such as azathioprine or cyclosporine may increase the risk of serious infections.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of baricitinib states that concurrent use of baricitinib with biologic DMARDs or potent immunosuppressants is not recommended.(1)
DISCUSSION: Most patients who developed serious infections while being treated with baricitinib were on concomitant immunosuppressants like methotrexate and corticosteroids. The combination of baricitinib with other biologic DMARDs has not been studied.(1)
Immunosuppressives; Immunomodulators/Deuruxolitinib
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Deuruxolitinib, immunosuppressives, and immunomodulators all suppress the immune system.(1)
CLINICAL EFFECTS: Concurrent use of deuruxolitinib and potent immunosuppressants may increase the risk of serious infections.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of deuruxolitinib states that concurrent use of deuruxolitinib with other JAK inhibitors, biologic immunomodulators, cyclosporine or other potent immunosuppressants is not recommended.(1) If concurrent use cannot be avoided, patients should be monitored for signs and symptoms of infection. If a patient develops a serious or opportunistic infection, interrupt deuruxolitinib treatment until the infection is controlled.
DISCUSSION: Serious infections have been reported in patients receiving treatment with deuruxolitinib.(1)
Immunosuppressives; Immunomodulators/Inebilizumab
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Inebilizumab, immunosuppressives, and immunomodulators all suppress the immune system.(1)
CLINICAL EFFECTS: Concurrent use of inebilizumab with immunosuppressive or immunomodulating agents may result in myelosuppression including neutropenia resulting in an increased risk for serious infections.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of inebilizumab states that the concurrent use of inebilizumab with immunosuppressive agents, including systemic corticosteroids, may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1)
DISCUSSION: Inebilizumab has not been studied in combination with other immunosuppressants. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents. The most common infections reported by inebilizumab treated patients in the randomized and open-label clinical trial periods included urinary tract infections (20%), nasopharyngitis (13%), upper respiratory tract infections (8%), and influenza (7%). Although there been no cases of Hepatitis B virus reactivation or progressive multifocal leukoencephalopathy reported in patients taking inebilizumab, these infections have been observed in patients taking other B-cell-depleting antibodies.(1)
Immunosuppressives; Immunomodulators/Ritlecitinib
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Ritlecitinib, immunosuppressives, and immunomodulators all suppress the immune system.
CLINICAL EFFECTS: Concurrent use of ritlecitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of ritlecitinib states that concurrent use of ritlecitinib with other JAK inhibitors, biologic immunomodulators, cyclosporine or other potent immunosuppressants is not recommended.(1)
DISCUSSION: Serious infections have been reported in patients receiving ritlecitinib. Reported infections included appendicitis, COVID-19 infection (including pneumonia), and sepsis. Reports of viral reactivation, including herpes virus reactivation was reported in clinical studies with ritlecitinib.(1)
Immunosuppressives; Immunomodulators/Tofacitinib
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Concurrent use of tofacitinib and azathioprine, other biologic disease-modifying antirheumatic drugs (DMARDs), or potent immunosuppressants may result in additive or synergistic effects on the immune system.(1)
CLINICAL EFFECTS: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants use may increase the risk of serious infections.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: Tofacitinib should not be used concurrently with azathioprine, other biologic DMARDs, or cyclosporine.(1) Patient should be monitored for decreases in lymphocytes and neutrophils. Therapy should be adjusted based on the indication. - For all indications: If absolute neutrophil count (ANC) or lymphocyte count is less than 500 cells/mm3, discontinue tofacitinib. - For rheumatoid arthritis or psoriatic arthritis and absolute neutrophil count (ANC) 500 to 1000 cells/mm3: interrupt dosing. When ANC is greater than 1000 cells/mm3, resume Xeljanz 5 mg twice daily or Xeljanz XR 11 mg once daily. - For ulcerative colitis and ANC 500 to 1000 cells/mm3: -If taking Xeljanz 10 mg twice daily, decrease to 5 mg twice daily. When ANC is greater than 1000 cells/mm3, increase to 10 mg twice daily based on clinical response. -If taking Xeljanz 5 mg twice daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 5 mg twice daily. -If taking Xeljanz XR 22 mg once daily, decrease to 11 mg once daily. When ANC is greater than 1000 cells/mm3, increase to 22 mg once daily based on clinical response. -If taking Xeljanz XR 11 mg once daily, interrupt dosing. When ANC is greater than 1000 cells/mm3, resume 11 mg once daily. - For polyarticular course juvenile idiopathic arthritis (pcJIA) and ANC 500 to 1000 cells/mm3: interrupt dosing until ANC is greater than 1000 cells/mm3.(1)
DISCUSSION: Concurrent use of tofacitinib and azathioprine, other biologic DMARDs, or potent immunosuppressants may increase the risk of infection.(1) Serious infections due to bacterial, mycobacterial, invasive fungal, viral, or other opportunistic pathogens have been reported in patients receiving tofacitinib. Some patients presented with disseminated disease and were often taking concomitant immunomodulating agents. In the ulcerative colitis population, a greater risk of serious infections was seen with a higher tofacitinib dose. In 7 placebo-controlled rheumatoid arthritis trials (0-3 months exposure), the overall frequency of infections was 20% in the tofacitinib 5 mg twice daily group and 22% in the tofacitinib 10 mg twice daily group compared to 18% in the placebo group. Serious infections were reported in 11 patients (1.7 events per 100 patient-years) with a rate difference between treatment groups of 1.1 (-0.4, 2.5) events per 100 patient-years for both tofacitinib 5 mg twice daily and 10 mg twice daily. During 0-12 months exposure, serious infections were reported in 34 patients (2.7 events per 100 patient years) in the tofacitinib 5 mg twice daily group and 33 patients (2.7 events per 100 patient years) in the tofacitinib 10 mg twice daily group.(1)
Immunosuppressives; Immunomodulators/Upadacitinib
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Upadacitinib, immunosuppressives, and immunomodulators all suppress the immune system.
CLINICAL EFFECTS: Concurrent use of upadacitinib with immunosuppressives or immunomodulators may result in an increased risk of serious infections.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of upadacitinib states that concurrent use of upadacitinib with immunosuppressives or immunomodulators is not recommended.
DISCUSSION: Serious infections have been reported in patients receiving upadacitinib. Reported infections included pneumonia, cellulitis, tuberculosis, multidermatomal herpes zoster, oral/esophageal candidiasis, cryptococcosis. Reports of viral reactivation, including herpes virus reactivation and hepatitis B reactivation, were reported in clinical studies with upadacitinib.(1)
Myelosuppressives; Immunomodulators/Sodium Iodide I 131
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Sodium iodide I 131 can cause depression of the hematopoetic system. Myelosuppressives and immunomodulators also suppress the immune system.(1)
CLINICAL EFFECTS: Concurrent use of sodium iodide I 131 with agents that cause bone marrow depression, including myelosuppressives or immunomodulators, may result in an enhanced risk of hematologic disorders, including anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia. Bone marrow depression may increase the risk of serious infections and bleeding.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of sodium iodide I 131 states that concurrent use with bone marrow depressants may enhance the depression of the hematopoetic system caused by large doses of sodium iodide I 131.(1) Sodium iodide I 131 causes a dose-dependent bone marrow suppression, including neutropenia or thrombocytopenia, in the 3 to 5 weeks following administration. Patients may be at increased risk of infections or bleeding during this time. Monitor complete blood counts within one month of therapy. If results indicate leukopenia or thrombocytopenia, dosimetry should be used to determine a safe sodium iodide I 131 activity.(1)
DISCUSSION: Hematologic disorders including death have been reported with sodium iodide I 131. The most common hematologic disorders reported include anemia, blood dyscrasias, bone marrow depression, leukopenia, and thrombocytopenia.(1)
Selected Immunosuppressants/Leflunomide; Teriflunomide
SEVERITY LEVEL: 2-Severe Interaction: Action is required to reduce the risk of severe adverse interaction.
MECHANISM OF ACTION: Concurrent use of leflunomide or teriflunomide and potent immunosuppressants may result in additive or synergistic effects on the immune system.(1,2) Leflunomide is a prodrug and is converted to its active metabolite teriflunomide.(1)
CLINICAL EFFECTS: Concurrent use of leflunomide or teriflunomide with immunosuppressants may result in an increased risk of serious infections, including opportunistic infections, especially Pneumocystis jiroveci pneumonia, tuberculosis (including extra-pulmonary tuberculosis), and aspergillosis.
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: If leflunomide or teriflunomide is used concurrently with immunosuppressive agents, chronic CBC monitoring should be performed more frequently, every month instead of every 6 to 8 weeks. If bone marrow suppression or a serious infection occurs, leflunomide or teriflunomide should be stopped and rapid drug elimination procedure should be performed.(1,2)
DISCUSSION: Pancytopenia, agranulocytosis and thrombocytopenia have been reported in patients receiving leflunomide or teriflunomide alone, but most frequently in patients taking concurrent immunosuppressants.(1,2) Severe and potentially fatal infections, including sepsis, have been reported in patients receiving leflunomide or teriflunomide, especially Pneumocystis jiroveci pneumonia and aspergillosis. Tuberculosis has also been reported.(1,2)
Moderate Interaction: Assess the risk to the patient and take action as needed.
Immunosuppressives; Immunomodulators/Ustekinumab
SEVERITY LEVEL: 3-Moderate Interaction: Assess the risk to the patient and take action as needed.
MECHANISM OF ACTION: Ustekinumab, immunosuppressives, and immunomodulators all suppress the immune system.(1)
CLINICAL EFFECTS: Concurrent use of ustekinumab with immunosuppressive or immunomodulating agents may result in an increased risk for serious infections.(1)
PREDISPOSING FACTORS: None determined.
PATIENT MANAGEMENT: The US manufacturer of ustekinumab recommends caution because the concurrent use of ustekinumab with immunosuppressive agents may increase the risk of infection. If concurrent therapy is warranted, consider the risk of additive immune suppression and monitor based on prescribing information for both agents.(1)
DISCUSSION: Ustekinumab has not been studied in combination with other immunosuppressants in psoriasis studies. In psoriatic arthritis studies, concomitant methotrexate use did not appear to influence the safety or efficacy of ustekinumab. In Crohn's disease and ulcerative colitis studies, concomitant use of immunosuppressants or corticosteroids did not appear to influence the safety or efficacy of ustekinumab. If concurrent therapy is warranted, consider the potential for increased immunosuppressive risks from both agents.(1) The most common infections reported by ustekinumab treated patients in the clinical trial periods included nasopharyngitis(8%) and upper respiratory tract infection(5%). Serious bacterial, mycobacterial, fungal, and viral infections were observed in patients receiving ustekinumab. Cases of interstitial pneumonia, eosinophilic pneumonia, and cryptogenic organizing pneumonia resulting in respiratory failure or prolonged hospitalization have been reported in patients receiving ustekinumab.(1)
Contraindications
*Known hypersensitivity to diroximel fumarate or dimethyl fumarate, or to any excipients in the formulation.
*Concomitant use of dimethyl fumarate.
- Progressive multifocal leukoencephalopathy
There are no severe contraindications for this drug.
- Lymphopenia
Adverse reactions
Adverse reactions reported with diroximel fumarate in clinical studies were similar to those reported with dimethyl fumarate (a drug with the same active metabolite as diroximel fumarate). In patients receiving dimethyl fumarate, adverse reactions reported in >=10% of patients and >=2% more frequently than with placebo include flushing, abdominal pain, diarrhea, and nausea.
Less Frequent
- Abnormal hepatic function tests
- Hyperbilirubinemia
- Increased aspartate transaminase
- Lymphopenia
Rare or Very Rare
- Acute pancreatitis
- Anaphylaxis
- Angioedema
- Gastrointestinal hemorrhage
- Gastrointestinal obstruction
- Gastrointestinal perforation
- Herpes zoster
- Opportunistic fungal infection
- Opportunistic viral infection
- Progressive multifocal leukoencephalopathy
More Frequent
- Acute abdominal pain
- Diarrhea
- Flushing
- Nausea
Less Frequent
- Dyspepsia
- Proteinuria
- Skin rash
Rare or Very Rare
- Alopecia
- Eosinophilia
- Gastrointestinal ulcer
- Rhinorrhea
Precautions
No enhanced messaging available.
Safety and efficacy of diroximel fumarate have not been established in pediatric patients.
There are no adequate data on the developmental risk associated with the use of diroximel fumarate during pregnancy. However, data from a pregnancy registry, observational studies, and pharmacovigilance related to the use of dimethyl fumarate in pregnancy have not indicated an increased risk of major birth defects, miscarriage, or other adverse maternal or fetal outcomes with that agent. Most dimethyl fumarate exposures occurred during the first trimester of pregnancy and the rate of major birth defects was 3.6% among 362 live births and stillbirths.
Animal data suggest that diroximel fumarate may cause fetal harm. Adverse developmental effects (e.g., skeletal abnormalities, increased mortality, decreased body weights, neurobehavioral impairment) have been observed in the offspring of animals administered diroximel fumarate during or throughout pregnancy at clinically relevant drug exposures.
A registry that monitors outcomes in pregnant women exposed to diroximel fumarate exists. Patients may enroll in the registry by calling 1-833-569-2635 or visiting https://www.blossomspregnancyregistry.com/.
It is not known whether diroximel fumarate or its metabolites are distributed into human milk. The effects of diroximel fumarate on the nursing infant or on milk production also are not known. Consider the benefits of breast-feeding along with the woman's clinical need for diroximel fumarate and any potential adverse effects on the breast-fed infant from the drug or underlying maternal condition.
Clinical studies of diroximel fumarate did not include sufficient numbers of patients >=65 years of age to determine whether geriatric patients respond differently than younger adults.
ICD codes
| Code | Type | Description |
|---|---|---|
| Relapsing form of multiple sclerosis | ||
| G35 | ICD10CM | Multiple sclerosis |
| G35.A | ICD10CM | Relapsing-remitting multiple sclerosis |
| G35.C0 | ICD10CM | Secondary progressive multiple sclerosis, unspecified |
| G35.D | ICD10CM | Multiple sclerosis, unspecified |
| Secondary progressive multiple sclerosis | ||
| G35 | ICD10CM | Multiple sclerosis |
| G35.C | ICD10CM | Secondary progressive multiple sclerosis |
| G35.C0 | ICD10CM | Secondary progressive multiple sclerosis, unspecified |
| G35.C1 | ICD10CM | Active secondary progressive multiple sclerosis |
| G35.D | ICD10CM | Multiple sclerosis, unspecified |
ICD code information from First Databank (FDB).
Formulary status
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Last reviewed · Source: First Databank (FDB) drug data
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