An official website of the United States government
NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
Indication: For the adjunctive treatment of adult patients with severe active anti-neutrophil cytoplasmic autoantibody-associated vasculitis (granulomatosis with polyangiitis and microscopic polyangiitis) in combination with standard background therapy including glucocorticoids. Avacopan does not eliminate glucocorticoid use
CADTH recommends that Tavneos not be reimbursed by public drug plans as adjunctive treatment for adults with severe active antineutrophil cytoplasmic autoantibody-associated vasculitis (ANCA-AV) (granulomatosis with polyangiitis [GPA] and microscopic polyangiitis [MPA]).
ANCA-AV is a group of rare diseases that causes inflammation of small- and medium-sized veins and arteries and can often affect other organs in the body. It is expected that at least 80% of patients who do not receive treatment die within 1 year of diagnosis. With treatment, patients are still at a higher risk of serious infections and kidney failure due to worsening disease and/or because of treatment. The prevalence of ANCA-AV is estimated to be between 75 and 300 per million or approximately 1,700 to 2,500 total patients living in Canada.
Patients with ANCA-AV need effective treatments that reduce or eliminate the need for glucocorticoids and their side effects, prevent disease progression, and improve their HRQoL.
Treatment with Tavneos is expected to cost approximately $75,000 per patient per year.
The CADTH Canadian Drug Expert Committee (CDEC) recommends that avacopan not be reimbursed as adjunctive treatment for adults with severe active ANCA-AV (GPA and MPA) in combination with standard background therapy, including glucocorticoids (avacopan does not eliminate glucocorticoid use).
The ADVOCATE trial (N = 331) was a phase III, double-blind (DB), noninferiority, randomized controlled trial (RCT) in patients with ANCA-AV, which concluded that treatment with avacopan in combination with background therapy including glucocorticoids and immunosuppressants (IV or oral cyclophosphamide or IV rituximab) was noninferior to oral prednisone (60 mg tapered over 20 weeks) in combination with background therapy including glucocorticoids and immunosuppressants (IV or oral cyclophosphamide or IV rituximab) for achieving disease remission at week 26 and was superior for sustained disease remission at week 52. CDEC was unable to determine if avacopan fills an unmet therapeutic need, mainly because rituximab was not used as maintenance therapy in the ADVOCATE trial, and patients induced with IV rituximab did not receive any maintenance therapy, neither of which aligns with the current Canadian guidelines for the diagnosis and management of ANCA-AV. In addition, only the primary outcomes of disease remission at week 26 and sustained disease remission at week 52 were controlled for multiple testing; hence all other outcomes were at increased risk of type I error. Furthermore, the between-group differences for multiple secondary outcomes (week 4 Birmingham Vasculitis Activity Score [BVAS], urinary albumin/creatinine ratio [UACR], Vasculitis Damage Index [VDI], patients experiencing disease relapse, SF-36v2, and EQ-5D) were relatively small with wide confidence intervals (CIs). Therefore, the clinical and statistical significance of the differences between the treatment groups on these outcomes is unknown.
Patients expressed that they expect new treatments for ANCA-AV to be effective while reducing or eliminating the need for glucocorticoids and their associated side effects, and to improve HRQoL. Given that in the ADVOCATE trial, HRQoL measures were secondary end points not controlled for multiplicity, CDEC was unable to determine if avacopan had an impact on HRQoL. In addition, the impact of any differences in corticosteroid use did not indicate a meaningful difference in safety results between the treatment groups. CDEC concluded that available evidence for avacopan does not address these important unmet needs identified by the patients.
ANCA-AV is a group of rare, inflammatory disorders affecting mostly small- to medium-sized blood vessels, and includes GPA, MPA, and other vasculitides. ANCA-AV can vary from non–life-threatening to severe disease, where, in the latter, major organs are affected, and from limited (i.e., affecting a single organ) to systemic disease. Limited information exists in the literature about its incidence and prevalence in Canada. According to the clinical expert consulted by CADTH, the incidence of GPA and MPA together is estimated to be 10 to 50 cases per million per year and prevalence is estimated to be between 75 and 300 cases per million or approximately 1,700 to 2,500 total patients living in Canada. Patients with ANCA-AV are at risk of increased morbidity and mortality largely due to the disease causing irreversible inflammatory organ damage and the consequences of long-term and often high-dose immunosuppressant drugs and glucocorticoids. It is expected that at least 80% of patients who go untreated will die within 1 year of diagnosis and even with treatment, patients are at increased risk of developing malignancies, serious infection, and end-stage kidney disease largely due to progressive disease and/or as a consequence of treatment.
According to the 2020 Canadian Vasculitis Research Network (CanVasc) Consensus Recommendations for the Management of ANCA-AV, IV methylprednisolone pulses are recommended for patients with life-threatening ANCA-AV followed by oral prednisone for those with severe disease. Patients with life-threatening disease are given cyclophosphamide or rituximab for a minimum of 3 to 6 months with glucocorticoids to induce remission. Cyclophosphamide and rituximab have shown similar efficacy for inducing remission; however, cyclophosphamide has been associated with fertility issues, alopecia, and malignancies, and rituximab may be preferred for specific patients (e.g., children, young adults concerned with infertility, and older adults with poor health). It is recommended that tapering glucocorticoids should begin within 2 weeks of induction therapy with cyclophosphamide or rituximab to reduce glucocorticoid exposure and their associated risks. Once remission is achieved, patients should be transitioned to maintenance therapy, preferentially rituximab (or azathioprine or methotrexate when rituximab maintenance cannot be used). It has been emphasized in the literature and by the clinical expert consulted by CADTH that maintenance treatment should continue for at least 2 years and additional treatment should be considered for those in high-risk groups (e.g., anti-proteinase 3 [PR3]-ANCA, prior relapse, pulmonary involvement, or upper respiratory tract involvement). Currently, the CanVasc recommendations state that the optimal duration for low-dose glucocorticoid use once remission is achieved is unknown.
Avacopan has been approved by Health Canada for the adjunctive treatment of adults with severe active ANCA-AV (GPA and MPA) in combination with standard background therapy including glucocorticoids and does not eliminate glucocorticoid use. Avacopan is a complement 5a receptor antagonist. It is available as 10 mg capsules and the dosage recommended in the product monograph is 30 mg (3 oral capsules of 10 mg each) taken orally twice daily.
To make its recommendation, the committee considered the following information:
CADTH received 1 patient group submission from Vasculitis Foundation Canada, an organization that aims to increase disease awareness and research support for all forms of vasculitis. Vasculitis Foundation Canada invited its mailing list subscribers to complete an online survey and received input from 46 patients (35 with GPA and 11 with MPA) from Canada and the US who have experience using prednisone or avacopan. The patient group reported that GPA and MPA impact patients’ daily lives and that patients experience a host of physical manifestations that lead to chronic fatigue, mood swings, poor sleep, chronic infections, and stress due to fear of relapse. Patients treated with prednisone reported side effects that significantly affect quality of life, including body disfiguration, steroid-induced diabetes or hypertension, infections requiring medical care, anxiety, and depression. Vasculitis Foundation Canada reported that patients with GPA or MPA indicated a need for a treatment that improves symptoms and quality of life that would also result in a reduction or elimination of the use of prednisone.
The clinical expert consulted by CADTH stated that patients need treatments that result in sustained remission, limited organ damage (or allow for better recovery from damage), limit the risk of severe infections, require less time on treatment (treatment shorter than 24 months has been associated with unacceptable high rates of relapse to date), and are safe for use in special populations (i.e., pediatric, pregnant, and older adult populations). The expert added that the disease and current ANCA-AV treatments have significant impact on patients’ HRQoL and ability to work.
Per the clinical expert, avacopan would be used as a first-line treatment for adults with severe GPA or MPA in-line with the patient population for the ADVOCATE trial. Although patients with the most severe forms of disease were excluded from the trial, the expert suggested that these patients may also be candidates for the drug after the disease is controlled with high-dose glucocorticoids. In practice, the expert stated that avacopan would be administered to induce remission alongside IV or oral cyclophosphamide or IV rituximab with glucocorticoids. Once remission is achieved, the clinical expert noted that patients would usually receive appropriate maintenance therapy, such as rituximab at month 6 and every 6 months thereafter for at least 24 months of total treatment. There is currently a lack of clinical trial evidence for optimal patient management after 12 months of avacopan.
According to the expert, all adults with severe GPA or MPA could be treated with avacopan and it is not clear if there are any subpopulations who would respond better to the drug than other patients, given the available evidence.
The clinical expert noted that survival is the most important outcome. Other response measures include improvement of major organ disease (e.g., renal recovery, reduced use of mechanical ventilation), achieving remission (typically assessed at month 3, then month 6), and sustained remission (at months 12, 18, and 24 thereafter). The expert stated that it is also important to evaluate and limit the side effects caused by treatments. Although there are instruments to measure disease- and treatment-related changes in studies, the expert indicated that these are not used in routine clinical practice.
As was done in the ADVOCATE trial, the clinical expert stated that avacopan should be administered for 12 months and suggested that while the drug could be used for longer, there are limited data available for stopping the drug before 1 year or using it beyond that. According to the expert, discontinuing treatment should be considered if there are intolerable side effects, continual disease progression with clinical decline, or repeated relapses. Per the expert’s opinion, another reason to discontinue avacopan is if it does not allow for a lesser use of glucocorticoids.
As GPA and MPA are rare diseases and require close monitoring, the clinical expert indicated that patients should be referred to a specialist with expertise in the disease area. In the clinical expert’s opinion, a rheumatologist, nephrologist, general internal medicine specialist, respirologist, or intensive care unit doctor should be able to prescribe avacopan in a hospital setting, and it was noted that restricting the prescription to only rheumatologists or nephrologists with expertise in vasculitis would likely delay treatment initiation by many weeks. However, in community clinics, the expert believed it would be reasonable to restrict access to rheumatologists or nephologists with experience treating vasculitis.
The clinical expert emphasized that treatment with avacopan should be associated with a mandate to stop or significantly decrease glucocorticoids within the first weeks of initiating avacopan; otherwise, the continued use of avacopan should be clinically justified. Given the lack of long-term data, the expert expressed uncertainty in patient management after 12 months of avacopan and in the long-term outcomes after stopping the drug. Lastly, the clinical expert suggested that alongside the implementation of avacopan in Canada, it would be useful to set up a registry to track drug use and patterns of use, and to monitor safety and efficacy.
CanVasc, a Canadian research network for vasculitis, provided input for this review. The clinician group expressed similar views to those of the clinical expert consulted by CADTH.
Input was obtained from the drug programs that participate in the CADTH reimbursement review process. The following were identified as key factors that could potentially impact the implementation of a CADTH recommendation for avacopan:
The clinical experts consulted by CADTH provided advice on the potential implementation issues raised by the drug programs.
The ADVOCATE trial (N = 331) was a phase III, DB RCT designed to investigate the efficacy and safety of avacopan in patients with ANCA-AV that aimed to determine if avacopan could induce and sustain remission without chronic glucocorticoid use at the levels currently used in SOC regimens. The trial compared avacopan (30 mg orally twice daily) to prednisone (60 mg per day orally tapered over 20 weeks) with respective matching placebos in addition to SOC therapy (IV or oral cyclophosphamide followed by azathioprine or IV rituximab without maintenance treatment) over 52 weeks with an 8-week follow-up. Patients were permitted to receive nonprotocol-specified low-dosage oral glucocorticoids (10 mg per day or less) for the treatment of adrenal insufficiency or allergic reaction. Eligible patients included adults who had a clinical diagnosis of GPA or MPA, were ANCA positive for either anti-PR3 or antimyeloperoxidase antibodies, and had active disease at screening. Patients with limited or most severe disease (alveolar hemorrhage requiring mechanical ventilation or with an eGFR of less than 15 mL/min/1.73 m2 at baseline) were not eligible. The primary outcomes were the proportions of patients who achieved disease remission at week 26 and sustained disease remission at week 52. Key secondary outcomes included GTI, HRQoL (SF-36v2, 5-Level EQ-5D [EQ-5D-5L], and EQ Visual Analogue Scale [VAS]), the proportion of patients experiencing disease relapse, kidney function (eGFR, UACR), and systemic damage (VDI). Harms and notable harms identified in the CADTH systematic review protocol were also assessed.
At baseline, the mean age of patients was 60.9 years (SD = 14.5 years), more than half were male (56.5%), and most were white (84.3%). Most patients were newly diagnosed with ANCA-AV (69.4%) compared to having relapsing disease (30.6%), more than half of patients had GPA (54.8%) compared to MPA (45.2%), and less than half were positive for anti-PR3 antibodies (43.0%) compared to antimyeloperoxidase antibodies (57.0%).
Survival was not assessed as an efficacy outcome in the trial but was captured as deaths for harms outcomes. Hospitalizations were not assessed in the trial. Symptoms (e.g., fatigue) were not assessed as an efficacy outcome but some symptoms may have been captured as harms outcomes. Only the primary outcomes of disease remission at week 26 and sustained disease remission at week 52 were controlled for multiple testing.
Based on the intention-to-treat analyses, 72.3% (95% CI, 64.8% to 78.9%) of patients randomized to avacopan and 70.1% (95% CI, 62.5% to 77.0%) of patients randomized to prednisone achieved remission at week 26. The estimate of common difference in remission rates between groups was 3.4% (95% CI, –6.0% to 12.8%; noninferiority P < 0.0001 and superiority P = 0.2387). Findings for the per-protocol population were similar.
At week 52, 65.7% (95% CI, 57.9% to 72.8%) of patients randomized to avacopan and 54.9% (95% CI, 46.9% to 62.6%) of patients randomized to prednisone achieved sustained remission. The estimate of common difference in sustained remission rates between groups was 12.5% (95% CI, 2.6% to 22.3%; noninferiority P < 0.0001 and superiority P = 0.0066). Findings for the per-protocol population were similar.
For patients with renal disease at baseline (based on the BVAS renal component), the LSM difference in change from baseline between treatment groups for eGFR was 2.9 mL/min/1.73 m2 (95% CI, 0.1 mL/min/1.73 m2 to 5.8 mL/min/1.73 m2) at week 26, 3.2 mL/min/1.73 m2 (95% CI, 0.3 mL/min/1.73 m2 to 6.1 mL/min/1.73 m2) at week 52, and | || || || || || || || || || | || || || || || || || || || | at week 60. In total, 7 patients required dialysis during the trial: 3 patients (1.8%) in the avacopan group and 4 patients (2.4%) in the prednisone group.
For patients with renal disease (based on the BVAS renal component) and albuminuria (defined as a UACR of at least 10 mg/g creatinine) at baseline, the LSM difference between groups in change from baseline for UACR was 1.3 mg/g (95% CI, 1.0 mg/g to 1.6 mg/g) at week 26, 1.1 mg/g (95% CI, 0.9 mg/g to 1.5 mg/g) at week 52, and | || || || || || || || || || at week 60.
Based on the data assessed by the adjudication committee, the LSM difference in change from baseline between treatment groups for the VDI was 0.1 (95% CI, –0.1 to 0.3) at week 26, 0.0 (95% CI, –0.2 to 0.3) at week 52, and | || || || || || || || at week 60.
For patients who achieved remission at week 26 (n = 120 in the avacopan group and n = 115 in the prednisone group), | || || || || || || || || || of patients in the avacopan group and | || || || || || || | of patients in the prednisone group experienced disease relapse. The estimate of common difference in rates was | || || || || || || || || || . The hazard ratio was 0.46 (95% CI, 0.25 to 0.84) for avacopan versus prednisone. Due to the small number of patients who relapsed, the median time to relapse was not estimable and Kaplan-Meier estimates were not calculated. During the 8-week follow-up period, 3.8% of patients in the avacopan group and 4.5% of patients in the prednisone group experienced disease relapse.
The LSM difference between treatment groups for the GTI Cumulative Worsening Score was –11.0 (95% CI, –19.7 to –2.2) at week 13 and –16.8 (95% CI, –25.6 to –8.0) at week 26. The LSM difference between treatment groups for the GTI Aggregate Improvement Score was –13.3 (95% CI, –22.2 to –4.4) at week 13 and –12.1 (95% CI, –21.1 to –3.2) at week 26.
The LSM difference in change from baseline between treatment groups for the SF-36v2 Mental Component Summary was 1.6 (95% CI, –0.6 to 3.8) at week 26, 1.7 (95% CI, –0.5 to 3.9) at week 52, and | || || || || || || | at week 60. The LSM difference between treatment groups for the SF-36v2 Physical Component Summary was 3.1 (95% CI, 1.2 to 5.0) at week 26, 2.4 (95% CI, 0.4 to 4.3) at week 52, and | || || || || || || | at week 60.
The LSM difference in change from baseline between treatment groups for the EQ-5D VAS was 3.6 (95% CI, –0.1 to 7.2) at week 26, 5.9 (95% CI, 2.3 to 9.6) at week 52, and | || || || || || || | at week 60. The LSM difference between treatment groups for the EQ-5D-5L index score was 0.0 (95% CI, 0.0 to 0.1) at week 26, 0.1 (95% CI, 0.0 to 0.1) at week 52, and | || || || || || || | at week 60.
Nearly all patients in the avacopan (98.8%) and prednisone (98.2%) groups experienced at least 1 treatment-emergent adverse event (TEAE). The 3 most common TEAEs in the avacopan group were nausea (23.5% with avacopan versus 20.7% with prednisone), peripheral edema (21.1% with avacopan versus 24.4% with prednisone), and headache (20.5% with avacopan versus 14.0% with prednisone). The 3 most common TEAEs in the prednisone group were peripheral edema, arthralgia (22.0% with prednisone versus 18.7% with avacopan), and muscle spasms (22.6% with prednisone versus 10.8% with avacopan).
Overall, 42.2% of patients in the avacopan group and 45.1% of patients in the prednisone group experienced a serious adverse event. The most common serious adverse events were ANCA-positive vasculitis (7.2% with avacopan versus 12.2% with prednisone) and pneumonia (5.4% with avacopan versus 5.5% with prednisone).
In total, 16.3% of patients in the avacopan group and 17.1% of patients in the prednisone group stopped treatment due to adverse events. The most common reason was ANCA-positive vasculitis (2.4% with avacopan versus 4.9% with prednisone) and other reasons occurred at a frequency of less than 2% for either group.
Six patients died during the treatment period in the ADVOCATE trial (2 patients receiving avacopan versus 4 patients receiving prednisone).
Treatment-emergent infections were reported among 68.1% and 75.6% of patients in the avacopan and prednisone groups, respectively. Serious treatment-emergent infections were reported among 13.3% and 15.2% of patients in the avacopan and prednisone groups, respectively, of which pneumonia was the most common serious infection–related TEAE (4.8% and 3.7%, respectively). Infections resulted in 9 patients withdrawing from the trial and 3 deaths.
Elevated alanine aminotransferase was reported by 4% and 2% of patients in the avacopan and prednisone groups, respectively; elevated aspartate aminotransferase was reported in 2% and 0% of patients in the respective groups; and elevated blood bilirubin was reported in 2% of patients in the avacopan group and 1% of patients in the prednisone group.
Acute myocardial infarction was reported by 1.2% of patients in the prednisone group and 0.6% of patients in the avacopan group, while cardiac failure was reported by 1.2% of patients in the avacopan group (and none in the prednisone group). Cardiac vasculitis was not reported in the trial.
Nausea was reported by 23.5% and 20.7% of patients in the avacopan and prednisone groups, respectively; diarrhea was reported by 15.1% and 14.6% of patients in the respective groups; vomiting was reported by 15.1% and 12.8% of patients, respectively; and dyspepsia was reported by 3.0% and 6.1% of patients, respectively.
Angioedema was reported by 1.2% of patients in the avacopan group (and none in the prednisone group).
The first notable limitation with the ADVOCATE trial was that rituximab was not used as maintenance therapy and patients induced with rituximab did not receive any maintenance therapy, neither of which aligns with the current Canadian guidelines for the diagnosis and management of ANCA-AV, which recommend using rituximab as first-line SOC maintenance therapy. This was due to rituximab not being approved as a maintenance therapy when the protocol for the ADVOCATE trial was being developed. Furthermore, it is unclear if the addition of avacopan to rituximab maintenance therapy would make a meaningful difference if these treatments were to be used in clinical practice today and there is currently a lack of clinical data to inform this. The second major limitation was the trial’s use of nonstudy immunosuppressants (19.7%) and glucocorticoids (89.1%). Nonstudy medication use is problematic for quantifying the effect of avacopan treatment alone for both efficacy and harms outcomes, and data for those who did not use glucocorticoids were unavailable. The Health Canada indication has specified avacopan as an add-on or adjunctive therapy to standard treatment rather than a glucocorticoid-sparing drug. These deviations from currently recommended SOC maintenance therapy and from the protocol likely biased the results, though the magnitude and direction of the bias are unknown. Other issues included the relatively large number of discontinuations from treatment (more than 20% in either group), which resulted in missing data for nearly all outcomes; multiple outcome measures not being validated for ANCA-AV; and the absence of published minimal important differences for this population.
Patients with ANCA-AV who have only ever had negative antibody results as well as those with very severe disease were excluded from the ADVOCATE trial and it is uncertain if the results of the trial can be generalized to patients with these characteristics. Also, the apparent difference in glucocorticoid use between treatment groups is more likely attributable to the trial design rather than a change in disease activity; for example, if avacopan was effectively controlling ANCA-AV. The instruments used in the ADVOCATE trial are not used in clinical practice, secondary outcomes were not controlled for multiplicity, and between-group differences for multiple secondary outcomes (week 4 BVAS, UACR, VDI, patients experiencing disease relapse, SF-36v2, and EQ-5D) were relatively small with wide CIs. Lastly, there was no rationale for the trial duration being 52 weeks or the follow-up being 8 weeks, and it is uncertain what long-term (beneficial or harmful) effects there are after discontinuing avacopan treatment. There was no indication from the trial about what posttreatment strategies should be used to manage patients with ANCA-AV and there is a lack of data informing this or whether avacopan can be continued for longer than 12 months.
Summary of Economic Evaluation.
CADTH identified the following key limitations with the sponsor’s analysis: the sponsor may have inaccurately estimated the total population eligible for treatment with avacopan, the uptake of avacopan plus SOC is expected to be higher than that estimated by the sponsor, and the rate of adherence for GCs is expected to be lower than that estimated by the sponsor.
CADTH reanalyses increased the proportion of incident patients treated with avacopan, decreased the proportion of prevalent patients treated with avacopan, changed the market share of avacopan, and decreased the rate of adherence for GCs. Based on the CADTH reanalyses, the estimated budget impact from reimbursing avacopan is expected be $4,099,173 in year 1, $8,319,444 in year 2, and $10,130,799 in year 3, for a 3-year total budget impact of $22,549,415.
The sponsor filed a Request for Reconsideration for the draft recommendation for avacopan for the adjunctive treatment of adults with severe active ANCA-AV (GPA and MPA) in combination with standard background therapy including glucocorticoids. In their request, the sponsor identified the following issues:
In the meeting to discuss the sponsor’s Request for Reconsideration, CDEC considered the following information:
All stakeholder feedback received in response to the draft recommendation from clinician groups and the public drug programs is available on the CADTH website.
Dr. James Silvius (Chair), Dr. Sally Bean, Mr. Dan Dunsky, Dr. Alun Edwards, Mr. Bob Gagne, Dr. Ran Goldman, Dr. Allan Grill, Mr. Morris Joseph, Dr. Christine Leong, Dr. Kerry Mansell, Dr. Alicia McCallum, Dr. Srinivas Murthy, Ms. Heather Neville, Dr. Danyaal Raza, Dr. Emily Reynen, and Dr. Peter Zed.
Initial meeting date: March 24, 2023
Regrets: One expert committee member did not attend.
Conflicts of interest: None
Reconsideration meeting date: July 27, 2023
Regrets: Two expert committee members did not attend.
Conflicts of interest: None
Disclaimer: The information in this document is intended to help Canadian health care decision-makers, health care professionals, health systems leaders, and policy-makers make well-informed decisions and thereby improve the quality of health care services. While patients and others may access this document, the document is made available for informational purposes only and no representations or warranties are made with respect to its fitness for any particular purpose. The information in this document should not be used as a substitute for professional medical advice or as a substitute for the application of clinical judgment in respect of the care of a particular patient or other professional judgment in any decision-making process. The Canadian Agency for Drugs and Technologies in Health (CADTH) does not endorse any information, drugs, therapies, treatments, products, processes, or services.
While care has been taken to ensure that the information prepared by CADTH in this document is accurate, complete, and up-to-date as at the applicable date the material was first published by CADTH, CADTH does not make any guarantees to that effect. CADTH does not guarantee and is not responsible for the quality, currency, propriety, accuracy, or reasonableness of any statements, information, or conclusions contained in any third-party materials used in preparing this document. The views and opinions of third parties published in this document do not necessarily state or reflect those of CADTH.
CADTH is not responsible for any errors, omissions, injury, loss, or damage arising from or relating to the use (or misuse) of any information, statements, or conclusions contained in or implied by the contents of this document or any of the source materials.
This document may contain links to third-party websites. CADTH does not have control over the content of such sites. Use of third-party sites is governed by the third-party website owners’ own terms and conditions set out for such sites. CADTH does not make any guarantee with respect to any information contained on such third-party sites and CADTH is not responsible for any injury, loss, or damage suffered as a result of using such third-party sites. CADTH has no responsibility for the collection, use, and disclosure of personal information by third-party sites.
Subject to the aforementioned limitations, the views expressed herein are those of CADTH and do not necessarily represent the views of Canada’s federal, provincial, or territorial governments or any third-party supplier of information.
This document is prepared and intended for use in the context of the Canadian health care system. The use of this document outside of Canada is done so at the user’s own risk.
This disclaimer and any questions or matters of any nature arising from or relating to the content or use (or misuse) of this document will be governed by and interpreted in accordance with the laws of the Province of Ontario and the laws of Canada applicable therein, and all proceedings shall be subject to the exclusive jurisdiction of the courts of the Province of Ontario, Canada.
The copyright and other intellectual property rights in this document are owned by CADTH and its licensors. These rights are protected by the Canadian Copyright Act and other national and international laws and agreements. Users are permitted to make copies of this document for noncommercial purposes only, provided it is not modified when reproduced and appropriate credit is given to CADTH and its licensors.
Redactions: Confidential information in this document may be redacted at the request of the sponsor in accordance with the CADTH Drug Reimbursement Review Confidentiality Guidelines.
About CADTH: CADTH is an independent, not-for-profit organization responsible for providing Canada’s health care decision-makers with objective evidence to help make informed decisions about the optimal use of drugs, medical devices, diagnostics, and procedures in our health care system.
Funding: CADTH receives funding from Canada’s federal, provincial, and territorial governments, with the exception of Quebec.
Indication: For the adjunctive treatment of adult patients with severe active anti-neutrophil cytoplasmic autoantibody-associated vasculitis (granulomatosis with polyangiitis and microscopic polyangiitis) in combination with standard background therapy including glucocorticoids. Avacopan does not eliminate glucocorticoid use.
Sponsor: Otsuka Canada Pharmaceutical Inc.
Final recommendation: Do not reimburse
Copyright © 2023 - Canadian Agency for Drugs and Technologies in Health. Except where otherwise noted, this work is distributed under the terms of a Creative Commons Attribution-NonCommercial- NoDerivatives 4.0 International licence (CC BY-NC-ND).
Your browsing activity is empty.
Activity recording is turned off.
See more...
