Deucravacitinib

Mechanism of Action

Tyrosine kinase 2 (Tyk2) is one of the Janus kinase (Jak) enzymes, which are intracellular tyrosine kinases that activate the Jak–signal transducer and the transcription (Jak-STAT) pathway. The remaining Janus kinase enzymes (ie, Jak1, Jak2, Jak3) stimulate a broad range of immune and extra-immune pathways (eg, lipid metabolism). In contrast, Tyk2-mediated signaling is involved with relatively few immune pathways.

Tyk2 promotes the signaling of inflammatory cytokines involved in innate (eg, type I interferons) and adaptive (eg, interleukins 12 and 23) immune responses. Interleukin 23 (IL-23) is associated with the pathogenesis of psoriasis and psoriatic arthritis. This cytokine initiates and stimulates the proliferation of T_H17 cells, which secrete inflammation mediators such as tumor necrosis factor-alpha (TNF-α) and IL-17. These signal molecules stimulate epidermal cell production and secretion of cytokines and chemokines that recruit and activate cells of the innate immune system. This upregulated T_H17 cell activity causes sustained inflammation in the skin and joints, as seen in psoriatic arthritis.

The drug demonstrates a strong affinity for this domain, making it highly selective for Tyk2 compared to other tyrosine kinases. During in vitro studies, deucravacitinib manifested a 100- to 2000-fold selectivity for Tyk2 compared to Jak1, 2, and 3. Additionally, deucravacitinib exhibited minimal or no binding of Jak1, 2, and 3.

Deucravacitinib binds allosterically to the regulatory domain of Tyk2 (JH2, or pseudokinase), a region that is typically catalytically inactive. The drug induces an inhibitory conformation change involving the locking of Tyk2's JH2 (regulatory) domain with its JH1 (catalytic) domain. Thus, deucravacitinib traps the Tyk2 protein in an inactive state.[19][20] 

Inhibition of Tyk2 promotes downregulation of the IL-23 (T_H17), type I interferon, IL-12, and keratinocyte activation pathways. However, the precise mechanism linking Tyk2 inhibition to the effective treatment of moderate-to-severe plaque psoriasis is unknown.[3] In patients with psoriasis, deucravacitinib reduces the expression of psoriasis-associated genes in a dose-dependent fashion. This includes reducing type I IFN pathway-regulated genes and the IL-23 pathway. Deucravacitinib reduces IL-17A levels by 47% to 50%, IL-19 by 72%, and β-defensin by 81% to 84% after once-daily administration for 16 weeks. However, the mechanism linking these reduced inflammation marker levels to the clinical effects of deucravacitinib has not been established.

Additionally, the selectivity of deucravacitinib for Tyk2 reduces the risk of adverse reactions, giving the drug a favorable safety profile. When administered transdermally, deucravacitinib also demonstrates significant antioxidative properties.[21]

Pharmacokinetics

Absorption: Following an oral dose of deucravacitinib, the Cmax and AUC increased proportionally, exhibiting linear pharmacokinetics. The absolute bioavailability of deucravacitinib was 99%, and the median Tmax was achieved in 2 to 3 hours.[22] The PK of deucravacitinib and its major active metabolite (BMT-153261) were almost comparable between healthy controls and patients with psoriasis.[3] A once-daily 6 mg dosing regimen resulted in a steady-state Cmax and AUC of deucravacitinib of 45 ng/mL and 473 ng/mL, respectively. The same dose resulted in a steady-state Cmax and AUC₂₄ of BMT-153261 of 5 ng/mL and 95 ng·hr/mL, respectively.[3] No significant differences were observed after a calorie-dense, high-fat meal of 51 total kcal with an approximate macronutrient distribution of 33% carbohydrates, 15% protein, and 52% fat.[3] When administered with food, the Cmax and AUC of deucravacitinib were reduced by approximately 24% and 11%, respectively, and the Tmax was prolonged by 1 hour. When administered with food, Cmax and AUC of BMT-153261 were reduced by approximately 23% and 10%, respectively, and the Tmax was prolonged by 2 hours.

Distribution: At a steady state, the volume of distribution of deucravacitinib was 140 L. Eighty-two percent to 90% of deucravacitinib was protein-bound, and its blood-to-plasma concentration ratio was 1.26. Patient body weight, age, gender, race, and ethnicity did not have a clinically significant effect on systemic exposure to deucravacitinib.[23]

Metabolism: Deucravacitinib undergoes N-demethylation mediated by cytochrome P-450 (CYP) 1A2 to form the metabolite BMT-153261, which demonstrates comparable pharmacological activity to the parent drug. The circulating BMT-153261 accounts for approximately 20% of the systemic exposure of the total drug-related components. Deucravacitinib is also metabolized by CYP2B6, CYP2D6, carboxylesterase (CES) 2, and uridine glucuronyl transferase (UGT) 1A9.[3][20]

Elimination: The terminal half-life of deucravacitinib is 10 hours.[3] The renal clearance of deucravacitinib ranges from 27 to 54 mL/min. After administration of a single radiolabeled deucravacitinib dose, about 13% and 26% were excreted unchanged in urine and feces, respectively. Approximately 6% and 12% of this single dose were recovered as BMT-153261 in urine and feces, respectively.

Administration

Available Dosage Forms and Strengths

Deucravacitinib is available as a 6 mg oral tablet.

Each tablet contains the active ingredient deucravacitinib and the following inactive excipients: croscarmellose sodium, anhydrous lactose, magnesium stearate, hypromellose acetate succinate, silicon dioxide, and microcrystalline cellulose. In addition, the Opadry II Pink component of the coating contains the following inactive components: iron oxide yellow, iron oxide red, polyvinyl alcohol, polyethylene glycol, talc, and titanium dioxide.

Adult Dosage

The recommended dose is one 6 mg tablet taken once daily regardless of food.[3][24] The patient should not chew, crush, or cut the tablets.

Storage and Handling:

Deucravacitinib tablets are stored at 68 to 77 °F (20 to 25 °C); temperature excursions are permitted between 59 and 86 °F (15 to 30 °C). Deucravacitinib is chemically a free base; its molecular formula is C20H19D3N8O3. The molecular weight of this compound is 425.47 g/mol. Deucravacitinib is a powder in physical form and appears white to yellow. The solubility of deucravacitinib depends on the pH of the solvent. The solubility increases with decreasing pH. 

Specific Patient Populations

Renal impairment: Kidney function can significantly affect the Cmax of deucravacitinib. In patients with mild renal dysfunction (GFR 60 to 90 mL/min/1.73 m²), the Cmax was 14% lower compared to patients with normal kidney function (GFR >90 mL/min/1.73 m²). In patients with moderate renal impairment (GFR 30 to 60 mL/min/1.73 m²), the Cmax was 6% higher than patients with normal kidney function. There was no significant difference in Cmax in patients with severe renal failure (GFR <30 mL/min/1.73 m²) or end-stage renal disease (ESRD) (GFR <15mL/min/1.73 m²) on dialysis compared to patients with normal kidney function. No significant differences in the AUC of deucravacitinib were observed in patients with mild renal failure. However, the AUC was higher by 39%, 28%, and 34% in patients with moderate, severe, and end-stage kidney disease on dialysis, respectively. The Cmax of MBT-153261 was 11% and 8% lower in patients with mild and moderate renal impairment, respectively. In contrast, it was higher by 28% and 9% in patients with severe renal dysfunction and end-stage renal disease on dialysis treatment, respectively. Only 5.4% of the deucravacitinib dosage was removed from the circulation during dialysis procedures.

Hepatic impairment: No adjustments are recommended in patients with concomitant mild (Child-Pugh A) or moderate (Child-Pugh B) liver impairment. Deucravacitinib is not recommended for patients with severe hepatic dysfunction (Child-Pugh C).[3] Compared to patients with normal liver function, the Cmax of deucravacitinib was 4%, 10%, and 1% higher in patients with mild, moderate, and severe hepatic impairment, respectively. For similar patient groups, the area under the curve to infinity (AUC_inf) was 10%, 40%, and 43% higher. Compared to patients with normal liver function, the Cmax of BMT-153261 was 25%, 59%, and 79% lower in patients with mild (Child-Pugh Class A), moderate (Child-Pugh Class B), and severe (Child-Pugh Class C) hepatic dysfunction, respectively. For similar patient groups, the AUC_inf was 3%, 20%, and 50% lower.

Pregnancy considerations: The data available from the case studies on deucravacitinib use during pregnancy are not adequate to assess the drug-associated risk of major congenital malformations, loss of pregnancy (abortion), and unfavorable fetal and maternal outcomes.[3] In preclinical studies, no adverse effects were observed on the development of embryo and fetus with oral administration of deucravacitinib to animals such as rats and rabbits during the phase of organogenesis at doses that were 91 times higher than the maximum recommended human dosage (MRHD) of 6 mg once a day. If the patient conceives while on deucravacitinib, pregnancy is reported at the adverse event reporting line of the drug manufacturing company.

Breastfeeding considerations: Data on the secretion of deucravacitinib in human milk, its effects on lactogenesis, and its effects on breastfed infants are not available. During animal studies, deucravacitinib was found in the milk of rats. While prescribing deucravacitinib, the health benefits of breastfeeding infants and the clinical need for therapy must be weighed against the potential adverse effects on the breastfed child.[3]

Pediatric patients: The safety and effectiveness of deucravacitinib have not been established in the pediatric patient population.

Older patients: In one clinical trial, 1519 patients with plaque psoriasis received deucravacitinib therapy. Of these, 152 patients (10%) were 65 or older, and 21 patients (1.4%) were 75. During the first 16 weeks of observation, severe adverse reactions occurred in 80 patients older than 65 and 12 patients older than 75; these patients were administered deucravacitinib without switching treatment arms. This rate of severe reactions was determined to be significantly higher than in younger patients. These severe effects included infection and many required treatment discontinuation. No significant difference in efficacy was observed between older and younger adults.

Adverse Effects

Deucravacitinib has consistently demonstrated a safety profile.[3] The safety of deucravacitinib was assessed in 2 placebo-controlled and active-controlled (PSO-1 and PSO-2) clinical trials and an open-label-extension (OLE) trial in which patients could enroll after completing the PSO-1 or PSO-2 trials. A total of 1519 patients with moderate-to-severe plaque psoriasis received deucravacitinib 6 mg once daily. Of these, 1141 patients were exposed to deucravacitinib for at least 12 months.

At week 16 in the PSO-1 trial, significantly higher response rates were observed in patients receiving deucravacitinib compared to placebo or apremilast. Therapeutic efficacy improved with treatment longer than 16 weeks and was maintained through week 52. At week 16 in the PSO-2 trial, more than 50% of patients receiving deucravacitinib achieved superior clearing compared to apremilast. Across multiple efficacy endpoints, deucravacitinib consistently demonstrated superiority to apremilast and was well tolerated in patients with moderate-to-severe plaque psoriasis.[25] A large proportion of patients treated with deucravacitinib reported a Psoriasis Symptoms and Signs Diary (PSSD) symptoms score of 0 at week 16, indicating relief from itching, pain, stinging, burning, and skin tightness (8% in deucravacitinib group versus 1% in the placebo arm) in both clinical trials.[26]

The exposure-adjusted incidence rate for adverse events in patients who were treated with deucravacitinib from through week 52 without interchanging treatment arm did not increase in comparison with the rate reported during the first 16 weeks of therapy.

Most of the adverse reactions were mild in severity. Respiratory complications were the most common adverse events:

• Upper respiratory tract infections
• Nasopharyngitis
• Pharyngitis
• Sinusitis
• Rhinitis
• Rhinotracheitis
• Tracheitis
• Laryngitis
• Tonsillitis

Other adverse reactions included oral ulcers, stomatitis, and acne.[14][27] Herpes simplex occurred in less than 1% of patients in the deucravacitinib group.

Severe adverse reactions in patients treated with deucravacitinib included:

• Upper respiratory infections
• Creatine phosphokinase elevations
• Herpes simplex
• Mouth ulcers
• Folliculitis
• Acne

The rate of severe adverse reactions necessitating discontinuation of therapy in patients who were treated with deucravacitinib was 2.4%, in comparison with 3.8% for the placebo group.[28]

Infection: Deucravacitinib may increase the risk of infections. In the placebo-controlled 16-week period, infections were reported in 29% of the patients treated with deucravacitinib (116 events per 100 person-years) compared with 22% treated with the placebo (83.7 events per 100 person-years). Most infections were not serious, were in the mild to moderate severity category, and did not cause discontinuation of deucravacitinib therapy. During this same period, serious infections occurred in 5 patients (2.0 per 100 patient-years) in the deucravacitinib group and 2 patients (1.6 per 100 patient-years) in the placebo group. During the 52-week treatment period, pneumonia and COVID-19 were the most common serious infections reported.[3]

Malignancy: During the 52-week treatment phase of the PSO-1 and PSO-2 clinical trials with a total exposure of 986 patient-years to deucravacitinib, malignancies were observed in 3 patients who received deucravacitinib therapy (0.3 per 100 patient-years), including a case of breast cancer, hepatocellular carcinoma, and lymphoma after treatment for 24, 32, and 25 weeks, respectively.[3] During PSO-1, PSO-2, and the open-label extension (OLE) trials, 3 patients (0.1 per 100 patient-years) in total developed lymphoma after 25, 77, and 98 weeks of treatment with deucravacitinib.

Drug-Drug Interactions

Various studies have failed to demonstrate any clinically significant differences in the pharmacokinetics of deucravacitinib when co-administered with the following drugs:[3]

• Fluvoxamine (CYP1A2 inhibitor)
• Ritonavir (CYP1A2 inducer)
• Famotidine (H2 receptor antagonist)
• Rabeprazole (proton pump inhibitor)
• Cyclosporine (dual Pgp/BCRP inhibitor)
• Pyrimethamine (OCT1 inhibitor)
• Diflunisal (UGT 1A9 inhibitor)

Similarly, studies have failed to demonstrate any clinically significant differences in the pharmacokinetics of the drugs listed below when administered concomitantly with deucravacitinib:

• Norethindrone acetate and ethinyl estradiol (oral contraceptives)
• Rosuvastatin
• Methotrexate
• Mycophenolate mofetil (MMF)

Cytochrome P450 (CYP) enzymes: Deucravacitinib is not an inducer of CYP1(A2), CYP2(B6), or CYP3(A4) group of enzymes. Deucravacitinib is not an inhibitor of enzymes CYP1(A2), CYP2(B6), CYP2(C8), CYP2(C9), CYP2(C19), CYP2(D6), or CYP3(A4).

Carboxylesterase (CES) enzymes: Deucravacitinib is not a class CES(2) enzyme suppressor.

Uridine diphosphate (UDP)-glucuronosyltransferase (UGT) enzymes: Deucravacitinib is not a suppressor of enzymes UGT1(A1), UGT1(A4), UGT1(A6), UGT1(A9), or UGT2(B7).

Transporter enzymes: Deucravacitinib is a substrate of BCRP, OCT1, and Pgp, but not MATE1, MATE2K, NTCP, OAT1, OAT3, OATP, or OCT2. deucravacitinib is a suppressor of BCRP and OATP1B3 but deucravacitinib is not an inhibitor of BSEP, MATE1, MATE2-K, MRP2, NTCP, OATP1B1, OAT1, OAT3, OCT1, OCT2, or Pgp.

Contraindications

Deucravacitinib is contraindicated for any patient with a history of hypersensitivity to deucravacitinib or any excipients used in the formula. Deucravacitinib administration in combination with other potent immunosuppressants is not recommended.[1]

Warnings and Precautions

Hypersensitivity: Hypersensitivity reactions have been observed in patients on deucravacitinib therapy. If a clinically significant hypersensitivity reaction such as angioedema occurs, the appropriate treatment should be administered, and deucravacitinib should be permanently discontinued. 

Infections: Patients on deucravacitinib therapy are susceptible to infections and reactivation infections.[24] Respiratory tract infections and herpes simplex are the most common. Severe infections include pneumonia and COVID-19. Therefore, deucravacitinib is not recommended for patients with life-threatening or active infections, including a medical history of exposure to tuberculosis, a history of a severe or opportunistic infection, and underlying conditions that may predispose them to infections.

During and after deucravacitinib treatment, close patient monitoring for signs and symptoms of infection is required. If an infection develops, appropriate antimicrobial therapy is initiated, and the patient is closely monitored. Deucravacitinib therapy is suspended if the patient develops a dangerous infection, and the treatment can be resumed after the infection has resolved.

Viral reactivation: Clinical trials reported reactivation of latent herpes virus leading to herpes zoster and herpes simplex. In the 16-week-long placebo-controlled phase, herpes simplex infection was reported by 17 patients (6.8 per 100 patient-years) who were on deucravacitinib treatment and 1 patient (0.8 per 100 patient-years) who received a placebo.

A severe type of herpes infection affecting multiple dermatomes was reported in immunocompetent patients who were on deucravacitinib therapy. During PSO-1, PSO-2, and the open-label extension (OLE) trial, most of the patients who reported herpes zoster events while receiving deucravacitinib were younger than age 50.

The effect of deucravacitinib on the reactivation of chronic viral hepatitis is unknown. During screening, patients who tested positive for hepatitis B or C were not included in clinical trials. According to clinical guidelines, viral hepatitis should be screened and monitored for reactivation infection before initiating therapy and during treatment with deucravacitinib.[24] If signs of reactivation occur, consultation with a hepatitis specialist should be arranged. Deucravacitinib is not recommended for patients with active hepatitis B or C.

Tuberculosis: Deucravacitinib is a systemic therapy that inhibits tyrosine kinase 2, a member of the Jak family. Before initiating therapy with deucravacitinib, patients must be evaluated for latent and active tuberculosis (TB).[24] A blood-based interferon-gamma release assay (IGRA) can detect mycobacterium tuberculosis infection.

Deucravacitinib is contraindicated in patients with active TB. Starting therapy for latent TB before administering deucravacitinib is recommended. If the patient has a medical history of TB, latent or active, and an adequate course of therapy cannot be confirmed, initiating anti-TB treatment before administering deucravacitinib may be considered. Patients on deucravacitinib treatment should be monitored for signs and symptoms of active TB during and after treatment.

Malignancy: Various malignancies, including lymphomas, were reported in patients enrolled in clinical trials with deucravacitinib.[3] Clinicians should weigh the benefits versus risks for the patient before initiating or continuing treatment, particularly in patients with a known malignancy (other than resolved non-melanomatous dermatological cancers) and patients who develop a malignancy while receiving deucravacitinib therapy.

Rhabdomyolysis: Cases of rhabdomyolysis have been reported in patients receiving deucravacitinib, which resulted in therapy interruption or permanent discontinuation. Deucravacitinib was associated with a higher incidence of asymptomatic elevation in levels of creatine phosphokinase (CPK) and rhabdomyolysis compared to treatment with a placebo.[3] The discontinuation of deucravacitinib is needed if marked elevation in CPK levels occurs or myopathy is suspected or diagnosed. Patients should promptly report any unexplained symptoms, such as muscle aches, tenderness, weakness, malaise, or fever.

Immunizations: Before starting deucravacitinib therapy, all age-appropriate immunizations, including the herpes zoster vaccination, should be completed. The immune response to live or killed vaccines has not been established. Patients receiving deucravacitinib treatment should avoid live vaccines.

Jak inhibition: The involvement of Tyk2 in adverse reactions associated with Jak inhibitor therapy has not been well established. One randomized post-marketing safety trial studied the effect of a Jak inhibitor in patients with rheumatoid arthritis (RA). Along with at least one cardiovascular risk factor, higher rates of all-cause mortality were observed in patients aged 50 and older who received Jak inhibitor treatment compared to TNF blockers. All-cause mortality included sudden cardiovascular death, major cardiovascular adverse events, deep venous thrombosis, pulmonary embolism, overall thrombosis, and malignancies (excluding non-melanomatous dermatological cancers).

Monitoring

Patients on deucravacitinib require follow-up visits to evaluate their response to therapy. Close monitoring of the patients for prompt detection and effective management of adverse drug reactions such as infections, rhabdomyolysis, hepatic dysfunction, and hypertriglyceridemia is required.[24] In addition, patients are assessed for complications associated with psoriasis. At a dosage range up to 6 times the recommended daily dosage of 6 mg, deucravacitinib does not cause any clinically significant prolongation of QTc interval.[29]

Patients receiving deucravacitinib therapy should be monitored using the following markers:

• Triglycerides
• Lipids
• Liver enzymes
• Creatine phosphokinase
• Glomerular filtration rate

Triglycerides: Therapy with deucravacitinib is associated with increased triglyceride levels.[3] However, the effect of a rise in this parameter on morbidity and mortality due to cardiovascular conditions has been undetermined. When on deucravacitinib treatment, the serum triglyceride levels need to be evaluated periodically per the clinical guidelines for hyperlipidemia. The clinical management of patients with hyperlipidemia is done according to the management guidelines for hyperlipidemia.

Lipids: The increase in mean triglycerides level by 10.3 mg/dL was observed in the patients treated with deucravacitinib during the 16-week treatment period, and the reported increase was by 9.1 mg/dL during the 52-week treatment period.[3]

Liver enzymes: Deucravacitinib is associated with elevated serum aminotransferase levels, but no clinically apparent acute hepatic injury cases have been reported.[30] Per the routine protocol, liver enzymes should be evaluated at baseline and periodically in patients with known or suspected hepatic disorders. If hepatic enzymes increase while on deucravacitinib, and drug-induced hepatic injury is suspected, interruption of deucravacitinib therapy is necessary until the diagnosis of hepatocellular injury is excluded.

Creatine phosphokinase: In the placebo-controlled period of 16 weeks, elevated creatine phosphokinase (CPK) levels, including Grade 4 severity, were observed in 23 patients (9.3 per 100 patient-years) receiving deucravacitinib therapy and 5 patients (4.1 per 100 patient-years) who were on placebo treatment.[3]

Glomerular filtration rate: During the placebo-controlled 16-week period, for patients with moderate impairment of renal function (eGFR 30 to 59 mL/min) at baseline, reduction in GFR reductions were observed in 4 patients (1.6 per 100 patient-years) who were on deucravacitinib treatment, and 1 patient (0.8 per 100 patient-years) on placebo therapy. Two of the patients treated with deucravacitinib had worsening baseline proteinuria.[3]

Toxicity

Recommendations

No clinical data is available for experience with deucravacitinib overdosage. If overdosage occurs in any patients, it is recommended to contact the Poison Help line for additional management of the condition according to the drug overdosage protocol. The elimination of deucravacitinib by treatment with hemodialysis was small in extent, up to 5.4% of the dosage per dialysis therapy, and therefore, limiting the use of hemodialysis in the treatment of overdosage or intoxication with deucravacitinib. 

Various studies using rate models have demonstrated no carcinogenicity was observed in male or female rats that administered deucravacitinib orally at doses up to 15 mg/kg/day, which is 51-fold higher than the MRHD as per AUC comparison.[3] In rats of the female gender, deucravacitinib had no effects on parameters of reproduction such as mating, fertility, or early development of the embryo at orally administered doses up to 50 mg/kg/day which is 171-fold higher than the MRHD, according to the comparison of AUC. In the male rat, deucravacitinib had no effects on mating, sperm morphology, fertility, or early embryonic parameters of their offspring at orally administered doses up to 50 mg/kg/day, which is 224 times higher than the MRHD according to a comparison of AUC.

Enhancing Healthcare Team Outcomes

Psoriasis is a chronic, immune-mediated inflammatory disorder. The disease burden is equally distributed in both genders worldwide. This condition causes physical disfigurement, which has a profound psychosocial impact, leading to low self-esteem, stigmatization, and isolation. Additionally, it reduces the lifespan of patients due to associated comorbidities. The expensive and prolonged treatment imposes a substantial economic burden on the patient and healthcare system. The community needs safer and more effective treatment to address these issues. Deucravacitinib is a breakthrough in the targeted treatment of moderate-to-severe plaque psoriasis.[3] The interdisciplinary healthcare team must work together to ensure the therapeutic safety and efficacy of deucravacitinib.

Clinicians prescribe deucravacitinib to the appropriate patients when they verbally consent to the treatment plan, set realistic treatment goals, and provide information about the potential adverse events of the drug therapy. An initial consultation is an excellent opportunity to develop a positive rapport with the patients, promoting a healthy mindset and mental well-being. The specialists can enhance the care of patients by offering invaluable input and leveraging their expertise.

Pharmacists can verify the drug dosing and perform a drug interaction check. They can also provide information on drug storage at home. The pharmacist can recommend reading an FDA-approved patient "Medication Guide" before starting deucravacitinib therapy each time the prescription is renewed.

Nurses can educate patients on the proper administration of drugs. They can also monitor adverse reactions, perform preliminary assessments of therapeutic effectiveness during follow-up visits, and verify the patient's compliance with the pharmacotherapy.

Nurses and pharmacists must communicate openly with prescribing physicians to report or discuss any concerns related to deucravacitinib therapy or the patient's other drug regimen. Such collaborative, interdisciplinary healthcare team communication is necessary to optimize patient care.

The patients are counseled to immediately seek professional assistance upon experiencing adverse reactions. Patients with plaque psoriasis often experience major depression with a sense of lost control over their medical condition and routine lives. The interprofessional healthcare team plays a crucial role in empowering the patients by promoting a perception of control and demonstrating comprehensive and collaborative efforts. This approach facilitates positive healthcare outcomes in the patients receiving deucravacitinib therapy.