Exploring Novel Management Options for Alopecia Areata

ABSTRACT

Alopecia areata (AA) is a chronic autoimmune disease characterized by a breakdown of immune privilege, resulting in an inflammatory response to hair follicles that can cause hair loss. Beyond its visible manifestations, AA imposes a considerable psychosocial burden and substantial economic impact due to increased health care utilization.

There is no cure for AA, and management may be challenging due to the heterogeneic and recurrent nature of the disease. Attenuating the autoimmune response to hair follicles and stimulating hair regrowth in affected areas are key goals of AA treatment. Given its central role in mediating AA-related inflammation, the JAK-STAT pathway is a common target of current pharmacological strategies.

Three JAK inhibitors are currently FDA-approved for severe AA: baricitinib, ritlecitinib, and deuruxolitinib. The safety and efficacy of these agents have been demonstrated in phase 3 trials. To support optimal outcomes for patients, there is an opportunity to recognize AA as a complex, immune-mediated condition rather than just a cosmetic concern. Aligning managed care coverage criteria with this clinical perspective and facilitating timely access to therapy may help mitigate the long-term clinical and economic consequences of the disease.

Am J Manag Care. 2026;32(suppl 4):S43-S52. https://doi.org/10.37765/ajmc.2026.89904

For author information and disclosures, see end of text.

Introduction

Alopecia areata (AA) is a complex autoimmune disease that causes hair loss.¹ Approximately 0.2% of individuals in the US have AA, with many having moderate to severe disease that presents with greater amounts of hair loss.^1-4 Individuals with AA experience a higher prevalence of several autoimmune, cardiovascular, and psychiatric comorbidities and also experience negative impacts on health-related quality of life (HRQOL), psychosocial well-being, and functioning at work and school related to AA.^1,4-7

The pathogenesis of AA is thought to involve a breakdown of immune privilege that leads to an inflammatory response towards hair follicles that weakens hair shafts and causes hair loss.^1,8 The JAK-STAT pathway is pivotal to the inflammatory response following the collapse of immune privilege in AA.^9,10

There is no cure for AA. Conventional therapeutic modalities may be associated with limited efficacy, patient adherence, and treatment satisfaction.^9,11,12 However, in 2022, the FDA approved the first therapy for AA, the JAK inhibitor baricitinib, to treat adults with severe AA; as of 2024, 3 JAK inhibitors are indicated for treatment of severe AA.^13,14 Managed-care decision makers are encouraged to consider the barriers to AA treatment, including disease awareness and challenges related to coverage and cost of therapy, despite the significant psychosocial impact of the disease.^6,15

Disease Background

AA is an autoimmune disease involving hair loss that can occur suddenly and unpredictably with relapses and remissions.¹ Hair loss can be persistent; however, since the disease does not destroy hair follicles, patients usually retain the potential for hair regrowth.¹ AA can be characterized by the pattern and extent of hair loss into patchy AA (round or patchy small bald lesions), alopecia totalis (AT) (total loss of hair on the scalp), or alopecia universalis (AU) (total loss of all hair on the body) (Figure 1^16-18).¹

Most commonly, AA presents with small, well-defined patches of hair loss that may spontaneously resolve over time; however, about one-third of patients experience subsequent relapses, and progression to AT or AU occurs in up to 10% of all cases.^1,10,19 Furthermore, spontaneous remission is uncommon in patients with AT or AU.¹⁰

As of 2017, the annual incidence of AA in the United States (US) was 87.39 cases per 100,000 person-years, with AT and AU being less common (combined, 7.09 cases per 100,000 person-years).² The mean age of AA onset is between 25 and 36 years, with more than 80% of patients experiencing their first episode of hair loss by age 40.⁵ In the US, the prevalence of AA is approximately 0.2%.^2,3 The estimated prevalence of moderate to severe disease—sometimes defined as greater than 50% scalp involvement, including AT and AU—ranges from approximately 35% to 43% among patients with AA.^3,4,19 AA affects people of all ages, genders, and races. However, higher rates have been reported among women, adults, and people of certain races and ethnicities (eg, Asian, Black, Hispanic/Latino).^2,20 It is a complex, immune-mediated disease with genetic and environmental causes and triggers, including emotional or physical stress.¹

Pathogenesis

The normal human hair growth cycle involves active hair/follicular growth (anagen phase), regression/follicular involution (catagen phase), and follicular rest and shedding of hair follicles (telogen phase).⁹ Immune privilege of the anagen hair follicle involves several mechanisms that suppress cytotoxic immune attacks on the hair bulb.⁹ The pathogenesis of AA may involve the breakdown of this immune privilege.⁸ Without immune privilege, anagen hair follicles can undergo immune recognition and damage by autoreactive immune cells.⁹ This inflammatory response disrupts the hair follicle cycle, weakening hair shafts and causing hair loss.^1,8 During the active disease process in AA, hair follicles cannot progress beyond the early anagen phase.⁹ However, hair follicles are not destroyed.⁹

The JAK-STAT pathway plays a central role in downstream signaling of inflammatory cytokines (including interleukins [ILs], interferons [IFNs], and several growth factors) to maintain both innate and adaptive immunity.^9,10 The JAK-STAT pathway plays a key role in mediating and maintaining the inflammatory response to hair follicles following the collapse of immune privilege in AA (Figure 2).^9,10

Diagnosis and Classification

Diagnosis of AA is usually based on clinical observation and may be supplemented by additional diagnostic tools such as a hair pull test, trichoscopy (noninvasive microscopic imaging of hair follicles and the scalp), or biopsy.^1,21,22 Assessing disease severity is important to inform clinical decision-making.²¹ The Severity of Alopecia Tool (SALT) is a validated scale for assessing the amount of hair loss on the scalp, with scores ranging from 0 (no scalp-hair loss) to 100 (complete scalp-hair loss).²¹ The SALT score is used primarily in clinical trials; however, achieving a SALT score of 20 or lower—indicating substantial scalp hair regrowth for patients with severe AA—has been demonstrated as a clinically meaningful outcome in real-world treatment.^19,21,23 Other tools such as the Alopecia Areata Scale may be used to assess features such as hair loss in other locations (eg, eyebrows, eyelashes) and the impact of disease on psychosocial functioning and responsiveness to AA treatment.²¹

Comorbidities and Clinical Impact of AA

AA is associated with several autoimmune (eg, atopic dermatitis, psoriasis, rheumatoid arthritis, inflammatory bowel disease), cardiovascular (eg, metabolic syndrome, hypertension, hyperlipidemia), and psychiatric (eg, depression, anxiety) comorbidities.^1,4,24 AA may be associated with common autoimmune and inflammatory comorbidities via shared genetics and common immune pathways; furthermore, the relationship between AA and psychiatric comorbidities may be due to both genetic and environmental factors.²¹

Patients with AA have a higher burden of comorbid conditions than do those without AA.^24,25 A systemic review and meta-analysis of 102 studies estimated the odds of 149 comorbidities in 680,823 people with AA compared to 72,011,041 healthy controls.²⁴ AA was associated with increased odds of several broad disease categories, including more than triple the risk of comorbid ocular or thyroid conditions and more than twice the risk of comorbid connective tissue, autoimmune, or neurologic conditions (Table 1).²⁴

In addition, AA is associated with negative impacts on HRQOL and psychosocial well-being, especially among women and those experiencing greater than 25% hair loss.^1,5 Indeed, the impact of AA extends beyond cosmetic concerns and carries a considerable psychosocial burden (Figure 3).⁶ Results of a 2018 online survey of 216 adult patients with self-reported moderate to severe AA recruited from the National Alopecia Areata Foundation (NAAF) patient database highlighted the disease’s impact on self-esteem, mood, activities of daily living, relationships, and attendance and performance at work and school. For example, most respondents (85%) reported that coping with AA was a daily challenge, and more than half (56%) reported worries about hair regrowth (Figure 3). Further, patients reported withdrawing from activities (62%) and reducing interactions with friends (54%) after the first episode of hair loss. However, the survey response rate was low, and the design did not include a control population; further, data may not be generalizable to the entire US patient population.⁶

The risk of work absenteeism and unemployment is considerably higher among patients with AA compared with healthy controls; this may be a consequence of several factors, including the development of anxiety and depression after diagnosis, social withdrawal, and an increased number of medical visits.⁷ In addition, AA can lead to decreased confidence that can alter educational or career plans and may interfere with obtaining job promotions, finding employment, and attending work functions.⁷ For example, in the previously discussed 2018 online survey, 45% of 132 employed individuals reported work absenteeism due to AA.⁶ Furthermore, among 47 respondents attending school, 51% reported missing time from school as a result of AA.⁶ These patients also reported poor school performance (including failing, having to repeat academic years, and discontinuing education) because of distraction and distress associated with AA.⁶

Conventionally Used Therapies and Unmet Needs

As previously noted, there is no cure for AA.¹¹ Management of AA is challenging due to the heterogeneity and recurrent nature of the disease.^11,26

The main goal of AA treatment is to diminish the autoimmune response to hair follicles and stimulate hair regrowth in affected areas.¹¹ Factors that may inform treatment selection include disease severity, patient age, disease stability, and patient distress.²⁶

Current Treatments

Until 2022, there were no FDA-approved treatments for alopecia; thus, most treatment options for AA are used off label.^13,27 The most commonly used treatments are locally administered corticosteroids (via intralesional injection or topical therapy).⁹ Other therapeutic options include systemic corticosteroids, topical and systemic calcineurin inhibitors, immunotherapies, and hair-growth-stimulating solutions (eg, minoxidil).^27,28 Local therapies are used either as a first-line treatment or for those with limited hair loss, while systemic therapies may be appropriate for patients with extensive hair loss or rapid disease progression.²⁷ Treatment options beyond pharmacotherapies include cryotherapy, phototherapy, and nonmedical interventions such as microblading and wigs or other hair prosthetics.²⁶

Unmet Needs

It may take months of treatment to see considerable improvement with AA.²⁶ In addition, conventional AA treatment modalities studied in limited randomized controlled trials have produced variable efficacy for treating AA, and they are often associated with a wide range of potential adverse events (AEs).⁹ For example, topical steroids carry the risk of skin atrophy, depigmentation, and telangiectasias; topical cyclosporine use can cause folliculitis and hyperkeratosis; and topical minoxidil treatment may be associated with dermatitis, pruritus, and hair growth at distant sites. Systemic steroid use may be associated with weight gain, hyperglycemia, and adrenal suppression, whereas certain systemic immunomodulator treatments can cause myelosuppression, rash, nausea, diarrhea, and hepatotoxicity. There is space in the therapeutic landscape for more directed treatments to better target the disease’s pathology and minimize AEs.⁹

Treatment delays may impact future treatment responses, with worse clinical responses seen in patients with longer duration of AA.^29-31 Unfortunately, there are often delays in treatment after diagnosis; in a retrospective study including approximately 68,000 patients with AA, 40% of patients were not prescribed treatment in the year following diagnosis.⁴ The authors hypothesized that this delay may reflect both watchful waiting in some patients (due to the possibility of spontaneous hair regrowth) and disease progression in others.⁴ The previously discussed 2018 online survey also examined the treatment burden among patients with AA.⁶ Respondents described their treatment experience as highly unsatisfactory. Use of medical treatment declined after diagnosis, and patients reported that discontinuation of AA treatment was most commonly due to AEs and lack of efficacy.⁶

Low treatment adherence was seen in a retrospective claims-based study characterizing treatment patterns among 7703 adults and 595 adolescents in the US during the first year after diagnosis with AA (including AT and AU). Data from the IBM Marketscape Commercial Claims and Encounters Database and Medicare Supplemental and Coordination of Benefits Database between 2014 and 2019 were analyzed for patients who were diagnosed between 2015 and 2018. The study evaluated treatment patterns associated almost exclusively with conventional AA treatments. Approximately 60% of patients received second-line treatment (ie, switched treatment), and the mean (SD) duration of first-line treatment was 76.9 (65.3) days for adults and 64.3 (56.4) days for adolescents. Furthermore, the rate of adherence to medication was only 37% in adults and 34% in adolescents. Limitations to this analysis included the possibility of treatment misclassification and an inability to capture over-the-counter treatments or medications not covered by insurance, the assumption that patients took their medications as prescribed, and the potential lack of generalizability to patients on Medicaid or those with no insurance. Based on these results, the authors suggested that conventional AA therapies are inadequate and that alternative treatment options are needed. The authors also noted that JAK inhibitor use was low in the study, as the data used were from before approval of any JAK inhibitors for AA.¹²

JAK Inhibitors for AA

The known involvement of JAK signaling in the pathogenesis of AA (Figure 2) has led to the development and testing of several JAK inhibitors to treat the disease.^1,10 Inhibition of JAK phosphorylation prevents activation of STAT proteins.⁹ The resulting decrease in proinflammatory cytokines can restore normal development among arrested anagen hair follicles.^9,32

Over the past few years, 3 JAK inhibitors have been approved for the treatment of severe AA: baricitinib (Olumiant; Lilly USA) in 2022, ritlecitinib (Litfulo; Pfizer) in 2023, and, most recently, deuruxolitinib (Leqselvi; Sun Pharmaceutical Industries) in 2024 (Table 2).^13,14,33,34 All 3 JAK inhibitors carry an FDA boxed warning describing class-wide risks of serious infections, mortality, malignancy, major adverse cardiovascular events, and thrombosis, based largely on postmarketing safety data from rheumatoid arthritis populations treated with another JAK inhibitor.^14,33,34 In AA, phase 3 trials and integrated safety analyses to date have not demonstrated new or unexpected safety signals and have shown low absolute rates of these events, but the available data are still limited, and careful risk-benefit assessment and ongoing monitoring remain essential.^14,33-36

Baricitinib Clinical Trials

The efficacy of baricitinib was evaluated in the randomized, double-blind, placebo-controlled, phase 2/3 BRAVE-AA-1 (NCT03570749) and phase 3 BRAVE-AA-2 (NCT03899259) studies, which enrolled 1200 adult patients with severe AA (≥ 50% scalp hair loss as measured by the SALT for > 6 months).^14,37,38 In both trials, the primary end point was the proportion of patients who achieved 20% or less of scalp hair loss (ie, SALT score of ≤ 20) at week 36.¹⁴

In BRAVE-AA-1, 184 patients were randomly assigned to receive baricitinib, 2 mg once daily, whereas 281 patients were given baricitinib, 4 mg once daily, and 189 patients were given placebo.¹⁴ At week 36, a greater proportion of patients who received baricitinib, 2 or 4 mg, achieved a SALT score of 20 or lower compared with those given placebo (22% vs 35% vs 5%, respectively) (difference vs placebo: baricitinib, 2 mg, 16% [95% CI, 10%-23%]; baricitinib, 4 mg, 30% [95% CI, 23%-36%]). Additionally, a greater proportion of patients who received baricitinib, 2 or 4 mg, achieved a SALT score of 10 or lower (ie, ≤ 10% scalp hair loss) compared with those given placebo (13% and 26% vs 4%, respectively) (difference vs placebo: baricitinib, 2 mg, 9% [95% CI, 3%-15%]; baricitinib, 4 mg, 22% [95% CI, 16%-28%]). Results were similar in BRAVE-AA-2, which enrolled slightly fewer patients (baricitinib, 2 mg, 156 patients; baricitinib, 4 mg, 234 patients; placebo, 156 patients).¹⁴

Across both trials, 371 patients were randomly assigned to placebo, 365 patients to baricitinib, 2 mg, and 540 patients to baricitinib, 4 mg. Of these, 845 patients were treated with baricitinib for 1 year or longer. AEs reported in clinical trials among at least 1% of patients treated with baricitinib included upper respiratory tract infections, headache, acne, hyperlipidemia, creatine phosphokinase increase, urinary tract infection, liver enzyme elevations, folliculitis, fatigue, lower respiratory tract infections, nausea, genital candidal infections, anemia, neutropenia, abdominal pain, herpes zoster, and weight increase.¹⁴

All patients who completed BRAVE-AA-1 entered a long-term extension trial.^14,39 This study examined the effects of therapy withdrawal after 52 weeks of treatment with baricitinib, 2 or 4 mg.³⁹ Patients who were initially randomly assigned to receive either dose of baricitinib and who achieved a SALT score of 20 or lower at week 52 (regardless of duration of response) were then randomly assigned again 3:1 to continue taking their current dose of baricitinib or transition to placebo (ie, withdrawal). Of those initially given baricitinib, 4 mg, 85 patients continued treatment, and 30 transitioned to placebo; of those initially given baricitinib, 2 mg, 29 patients continued treatment, and 10 patients transitioned to placebo. At week 152, 90% of patients on the 4-mg dose and 89% of patients on the 2-mg dose maintained a SALT score of 20 or lower, whereas only 20% of those withdrawn from baricitinib, 4 mg, and 10% of those withdrawn from baricitinib, 2 mg, maintained a SALT score of 20 or lower. Withdrawal of therapy among patients with severe AA who achieved meaningful hair regrowth after 1 year of treatment with baricitinib resulted in almost all patients losing hair. Based on these data, therapy discontinuation was not recommended after achieving successful regrowth with 1 year of therapy.³⁹

Ritlecitinib Clinical Trials

The efficacy of ritlecitinib was evaluated in the phase 2b/3, randomized, double-blind, placebo-controlled ALLEGRO-2b/3 trial (NCT03732807) in 718 patients 12 years or older with severe AA (≥ 50% scalp hair loss, including AT and AU), who were randomly assigned to receive ritlecitinib once daily for 48 weeks.^33,40 The approval of ritlecitinib was based on results at 24 weeks in 130 patients who received ritlecitinib, 50 mg, compared with 131 patients who received placebo.³³

At week 24, a greater proportion of patients who received ritlecitinib, 50 mg, had a SALT score of 20 or lower compared to the placebo group (23.0% vs 1.6%, respectively; difference: 21.4% [95% CI, 13.4%-29.5%]).³³ Similar results were seen in those who achieved a SALT score of 10 or lower compared to patients given placebo (13.4% vs 1.5%; difference, 11.9% [95% CI, 5.4%-18.3%]).

The safety of ritlecitinib was evaluated in 3 randomized, placebo-controlled clinical trials and 1 long-term trial in 1628 patients 12 years or older with AA. Of these, 1011 patients were treated with ritlecitinib for 1 year or longer. AEs reported in at least 1% of patients in these trials included headache, diarrhea, acne, rash, urticaria, folliculitis, pyrexia, atopic dermatitis, dizziness, increased blood creatine phosphokinase, herpes zoster, decreased red blood cell count, and stomatitis. In addition, 2 patients (1.5%) treated with ritlecitinib, 50 mg, discontinued treatment due to AEs.³³

Interim efficacy and safety results up to 24 months have been published for patients enrolled in ALLEGRO-2b/3 who rolled over into the ongoing, phase 3 open-label ALLEGRO-LT study (NCT04006457). In all, 191 patients received 50 mg of ritlecitinib from treatment initiation, and 194 patients were given a 4-week ritlecitinib loading dose of 200 mg/day followed by 50 mg once daily. At 12 months, a SALT score of 20 or lower was achieved by 45.1% and 45.9% (observed) of patients in the ritlecitinib, 50 mg, and ritlecitinib, 200/50 mg, groups; in addition, this outcome was achieved respectively in 40.3% and 41.8% in last observation carried forward (LOCF). At 24 months, proportions increased to 60.8% and 63.1% (observed) and 46.1% and 50.8% (LOCF), respectively.⁴¹ No new safety signals were detected in this analysis.⁴¹

Deuruxolitinib Clinical Trials

The efficacy and safety of deuruxolitinib were assessed in the phase 3, multicenter, randomized, double-blind, placebo-controlled THRIVE-AA1 (NCT04518995) and THRIVE-AA2 (NCT04797650) trials involving adult patients with severe AA (≥ 50% scalp hair loss as measured by SALT for > 6 months).³⁴ The efficacy and safety of deuruxolitinib treatment was evaluated in 1209 adult patients across both trials, with patients randomly assigned to receive 8 or 12 mg of deuruxolitinib or placebo twice daily (5:3:2 in THRIVE-AA1 and 2:1:1 in THRIVE-AA2, respectively).^34,42,43 (Note that deuruxolitinib, 12 mg, is not an approved dosage,³⁴ and results are not reported).

At week 24, greater proportions of patients who received the 8-mg deuruxolitinib dose had a SALT score of 20 or lower compared with the placebo groups in both trials (THRIVE-AA1, 29% vs 1%; THRIVE-AA2, 32% vs 1%).³⁴ Additionally, compared with the placebo arm, significantly more patients receiving deuruxolitinib achieved an absolute SALT score of less than 20 from as early as week 8 (pooled data from THRIVE-AA1 and THRIVE-AA2; P < .001 at all assessed time points).⁴⁴

The safety of deuruxolitinib was evaluated in 1730 adult patients with severe AA across 3 randomized, placebo-controlled clinical trials (including a dose-ranging trial), 2 open-label trials, and 2 long-term extension trials. In total, 974 patients were exposed to either deuruxolitinib, 8 or 12 mg for at least 1 year; 104 patients were exposed for at least 3 years. AEs reported in at least 1% of 640 patients given 8 mg of deuruxolitinib twice daily were headache, acne, nasopharyngitis, increased blood creatine phosphokinase, hyperlipidemia, fatigue, increased weight, thrombocytosis, anemia, skin and soft tissue infections, neutropenia, and herpes.³⁴

Upon completion of the 24-week trials, patients were eligible to enroll in similarly designed long-term extension trials (NCT03898479 [N = 1099]; NCT05041803 [N = 407]).^34,45 The interim analysis of pooled results through 68 weeks of treatment with deuruxolitinib, 8 mg, showed continued improvement in hair regrowth over time (Figure 4).⁴⁵

Managed Care Considerations

There are several barriers to accessing appropriate care in AA. Low public awareness of the disease may limit understanding, contribute to stigma, and delay diagnoses and treatment.¹⁵ Affected patients may not realize that AA is an immune-mediated dermatologic disease rather than a purely cosmetic condition, leading to delays in seeking appropriate medical care. Furthermore, nonspecialist health care providers may lack awareness and understanding of AA, resulting in challenges with identifying AA-associated hair loss and potential failure to refer patients to dermatologists for clinical diagnosis and treatment. Providers, payers, and policymakers may not understand the holistic impact of AA on patients; this barrier may lead to limited treatment access and coverage.¹⁵ For example, fewer than half of patients (49%) in the 2018 online survey study reported having insurance coverage for AA treatment.⁶ The cost of treatment was a noted barrier among patients without insurance coverage.⁶

Indeed, patients with AA experience a substantial economic burden due to increased use of health care services. In a retrospective cohort study, the total direct medical cost of AA from the US third-party commercial payer perspective was evaluated by comparing costs from 14,340 patients with AA with those of 42,998 matched controls. Data from 2016 to 2018 were included for patients at least 12 years old, and costs were evaluated in the first year after diagnosis. Compared with matched controls, patients with AA had significantly higher all-cause medical costs that mostly were due to higher inpatient costs, the number and cost of emergency department and ambulatory visits, and the number and cost of prescriptions (all, P < .0001) (Figure 5). Limitations of this analysis included the possibility of incomplete, inaccurate, or missing claims data and inaccurate diagnostic coding; further, direct costs associated with AA treatment could not be separated from the costs of comorbidities associated with AA. Potential confounders included disease severity and multimorbidity, and results may not have applied to patients without commercial health plans. Additionally, this study was conducted before the FDA approval of any JAK inhibitors for AA.²⁵

Coverage of JAK inhibitor therapy was assessed in a separate online 2023 survey of 600 patients with AA (> 50% scalp involvement, 70.7%) identified through the NAAF.⁴⁶ Among respondents, 41.3% reported having no insurance coverage for JAK inhibitors, and only 25.6% reported full coverage for AA treatment with a JAK inhibitor. Among 172 patients reporting current or prior use of a JAK inhibitor, 52.9% reported delays due to the insurance approval process, and 49.5% reported that the delay worsened their AA, with 22% experiencing a delay of greater than 6 months. Furthermore, 19.8% of those currently or previously receiving treatment with a JAK inhibitor reported having to use financial savings to pay for treatment, and 12.2% reported having to give up necessities to pay for treatment.⁴⁶ (Note: This survey was distributed 14 months after FDA approval of baricitinib, 2 months after approval of ritlecitinib, and before approval of deuruxolitinib).^13,46 The study authors added that 45% of patients received off-label JAK inhibitor treatment; many respondents could have obtained JAK inhibitor treatment before FDA approval, which may have influenced perceptions of access and associated financial burden.⁴⁶ However, the authors emphasized that patients with AA may not try to obtain or may discontinue medical therapies such as JAK inhibitors due to concerns about cost, lack of insurance coverage, and associated economic burden.⁴⁶

Outside of JAK inhibitor therapies, other investigational treatments are being explored in clinical trials to treat AA.⁴⁷ These include diphenylcyclopropenone ointment (phase 3), coacillium topical solution (phase 2/3), and bempikibart subcutaneous (SC) injection, EQ101 intravenous injection, NXC-736 oral formulation, rezpegaldesleukin SC injection, and amlitelimab SC injection (all phase 2).⁴⁷

Conclusions

AA is associated with a profound psychosocial impact due to the visible nature of hair loss that leads to anxiety, depression, and impaired QOL in affected patients. These challenges are compounded by significant treatment barriers, including lack of disease awareness, delays in diagnosis and treatment, high out-of-pocket costs, and inconsistent insurance coverage for approved therapies.

For managed care professionals, addressing these barriers is critical to achieving positive health outcomes in patients with AA. By ensuring timely formulary inclusion, establishing clear and equitable coverage criteria, and prioritizing access to targeted therapies such as JAK inhibitors, managed care organizations can reduce the financial and psychological burdens on patients. Furthermore, managed care professionals can play a pivotal role by connecting patients with psychosocial support resources, educational materials, and community networks. This coordinated approach to patient care encompasses both clinical and supportive elements and is essential for improving the management of AA.

Authorship Affiliation: Clinical Operations, Capital Rx (LG), New York, NY; The Kimberly and Eric J. Waldman Department of Dermatology, Icahn School of Medicine at Mount Sinai (BU, EG, ML), New York, NY.

Source of Funding: This supplement was supported by Sun Pharmaceutical Industries, Inc.

Author Disclosures: Dr Guttman reports participating in consultancies or paid advisory boards with Sanofi. She also reports receiving grants from AbbVie, Aclaris Therapeutics, Amgen, AnaptysBio, Apollo Therapeutics, Arcutis Biotherapeutics, Bristol Myers Squibb, Concerto Biosciences, Galderma, GSK, ImageneBio, InCyte, LEO Pharma, Lilly, Opsidio, Pfizer, Regeneron, Sanofi, Xencor, and Q32 Bio. Dr Lebwohl reports participating in consultancies or paid advisory boards with AbbVie, Added Health, Aikium, Almirall, AltruBio, Alumis, Amgen, Apogee, Arcutis Biotherapeutics, AstraZeneca, Atomwise, Avotres Therapeutics, Boehringer Ingelheim, Bristol Myers Squibb, Castle Biosciences, Celltrion, Corevitas, Dermavant Sciences, Dermsquared, Edessa, Evommune, Facilitation of International Dermatology Education, Forte Biosciences, Galderma, Genentech, Johnson & Johnson, InCyte, LEO Pharma, Lilly, Mayne Pharmaceuticals, Meiji Seika Pharma, Mindera, Mirium Pharmaceuticals, Moonlake Immunotherapeutics, Oruka Therapeutics, Pfizer, Revolo Biotherapeutics, Sanofi-Regeneron, Seanergy Dermatology, Strata Oncology, Sun Pharma, Takeda, Trevi Therapeutics, and Verrica Pharmaceuticals. He has received grants from AbbVie, Arcutis Biotherapeutics, Avotres, Boehringer Ingelheim, Bristol Myers Squibb, Cara Therapeutics, Clexio Biosciences, Dermavant Sciences, InCyte, Inozyme Pharma, Johnson & Johnson, Lilly, Oruka Therapeutics, Pfizer, Sanofi-Regeneron, and UCB. He also reports receiving honoraria from Aikium, Almirall, AltruBio, Amgen, Apogee, Arcutis Biotherapeutics, AstraZeneca, Atomwise, Avotres, Boehringer Ingelheim, Bristol Myers Squibb, Castle Biosciences, Celltrion, CorEvitas Clinical Registries, Dermavant Sciences, Dermsquared, Evommune, Forte Biosciences, Galderma, Genentech, GoodRx–Mayne Pharma, InCyte, International Dermatology Education Foundation, LEO Pharma, Meiji Seika Pharma, Mindera, Mirum, Oruka Therapeutics, Pfizer, Revolo Biotherapeutics, Sanofi-Regeneron, Seanergy Dermatology, Stratpharma, Sun Pharma, Takeda, Trevi Therapeutics, and Verrica Pharmaceuticals. Dr Ungar reports receiving grants from Bristol Myers Squibb, InCyte, Pfizer, Rapt Therapeutics, and Sanofi. He also reports participating in consultancies or paid advisory boards with AbbVie, Arcutis Biotherapeutics, Apogee, Bristol Myers Squibb, Botanix Pharmaceuticals, Castle Biosciences, Ebla Holdco, Fresenius Kabi, Galderma, Johnson & Johnson, Leo Pharma, Lilly, Nektar Therapeutics, Pfizer, Primus Pharmaceuticals, Sanofi, Sun Pharma, UCB, Veradermics, and VRG Therapeutics.

Authorship Information: Concept and design (BU, EG, ML); analysis and interpretation of data (EG, ML); drafting of the manuscript (EG, LG); critical revision of the manuscript for important intellectual content (BU, EG, LG, ML); administrative, technical, or logistic support (LG); supervision (BU, EG).

Address Correspondence to: Benjamin Ungar, MD, 5 East 98^th Street, Fifth Floor. New York, NY, 10029. Email: benjamin.ungar@mountsinai.org.

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