Abrahim Abduelmula, BScN1; Brian D. Rankin, MD, PhD2; Asfandyar Mufti, MD, FRCPC3; Jensen Yeung, MD, FRCPC3-6; Vimal H. Prajapati, MD, FRCPC2,6-10

1Faculty of Medicine, University of Western Ontario, London, ON, Canada
2Division of Dermatology, Department of Medicine, University of Calgary, Calgary, AB, Canada
3Division of Dermatology, Department of Medicine, University of Toronto, ON, Canada
4Women’s College Research Institute, Women’s College Hospital, Toronto, ON, Canada
5Sunnybrook Health Sciences Centre, Toronto, ON, Canada
6Probity Medical Research, Waterloo, ON, Canada
7Dermatology Research Institute, Calgary, AB, Canada
8Skin Health & Wellness Centre, Calgary, AB, Canada
9Section of Community Pediatrics, Department of Pediatrics, University of Calgary, Calgary, AB, Canada
10Section of Pediatric Rheumatology, Department of Pediatrics, University of Calgary, Calgary, AB, Canada

Conflict of interest:
Abrahim Abduelmula has no relevant disclosures. Brian D. Rankin has no relevant disclosures. Jensen Yeung has been an advisor, consultant, speaker, and/or investigator for AbbVie, Allergan, Amgen, Astellas, Boehringer Ingelheim, Celgene, Centocor, Coherus, Dermira, Eli Lilly, Forward, Galderma, GSK, Janssen, LEO Pharma, Medimmune, Merck, Novartis, Pfizer, Regeneron, Roche, Sanofi Genzyme, Sun Pharma, Takeda, UCB, Valeant, and Xenon. Vimal H. Prajapati has been an advisor, consultant, speaker, and/or investigator for AbbVie, Actelion, Amgen, AnaptysBio, Aralez, Arcutis, Arena, Aspen, Bausch Health, Boehringer Ingelheim, Bristol Myers Squibb, Celgene, Cipher, Concert, Dermavant, Dermira, Eli Lilly, Galderma, GSK, Homeocan, Incyte, Janssen, LEO Pharma, Medexus, Nimbus Lakshmi, Novartis, Pediapharm, Pfizer, Regeneron, Reistone, Sanofi Genzyme, Sun Pharma, Tribute, UCB, and Valeant.

Funding sources: None.

Abstract:
Atopic dermatitis (AD) is a common, chronic, recurrent, immune-mediated inflammatory skin disease. Targeted treatment options remain limited. Tralokinumab (Adtralza®) is a promising, new systemic therapy that inhibits interleukin-13. It was recently approved by Health Canada and the US FDA for the treatment of moderate-to-severe AD in adults and may be used alone or with topical corticosteroids. Herein, we review the efficacy and safety of tralokinumab in adults, as demonstrated in clinical trials.

Keywords:
Adtralza®, tralokinumab, immunomodulator, therapeutics, biologic, atopic dermatitis, eczema, clinical trial

Introduction

Atopic dermatitis (AD) is a common, chronic, recurrent, immune-mediated inflammatory skin disorder affecting between 5-10% of adults, with moderate-to-severe disease accounting for approximately 20-30% of cases.1,2 This condition can have a significant negative impact on psychosocial well-being, health-related quality of life (QoL), and work/school productivity. In addition, uncontrolled AD is associated with a substantial financial burden on the patient and their family as well as the health care system.3

Topical therapies are employed as first-line treatment for the majority of AD cases, but lack of response can necessitate the use of phototherapy and/or systemic therapies. With respect to systemic therapies, recent advances have led to the development of new targeted treatments, of which four are now approved by Health Canada and the US FDA for moderate-to-severe AD. This includes two biologics (dupilumab [Dupixent®], an interleukin (IL)-4/IL-13 inhibitor, and tralokinumab [Adtralza®], an IL-13 inhibitor) and two small molecules (upadacitinib [Rinvoq®] and abrocitinib [Cibinqo®], both selective Janus kinase 1 [JAK1] inhibitors).

Background

Tralokinumab is a fully human immunoglobulin G4 (IgG4) monoclonal antibody that binds with high affinity to IL-13, thereby blocking its interaction with the IL-13Rα1/IL-4Rα1 heterodimer and IL-13Rα2 homodimer receptor complexes and subsequently leading to downstream STAT-6 inhibition.4 The latter results in reduced inflammation, improved skin barrier function (reductions in epidermal thickness and increased epithelial barrier integrity), as well as restoration of the microbiome (a near 10-fold reduction in Staphylococcus aureus colonization of the skin).4,5

Tralokinumab may be given alone or in combination with a topical corticosteroid (TCS).6,7 It was approved by both Health Canada and the US FDA in 2021 for the treatment of moderate-to-severe AD in adult patients whose disease is not adequately controlled with prescription topical therapies or when those prescription topical therapies are not advisable.6 Available as a single-use prefilled syringe containing 150 mg of tralokinumab in 1 mL solution (150 mg/mL), tralokinumab is administered as a subcutaneous (SC) injection.6 The recommended dosage for adult patients is an initial 600 mg loading dose followed by 300 mg maintenance doses every other week (Q2W). According to the product monograph, the prescriber may choose to administer tralokinumab every fourth week (Q4W) in adult patients who achieve clear or almost clear skin after 16 weeks of treatment; however, there is an increased probability that maintenance efficacy may be decreased with Q4W dosing.6

Non-medicinal ingredients of the product include acetic acid, polysorbate 80, sodium acetate trihydrate, sodium chloride, and water. No published data is currently available for its use in pediatric or pregnant patients, and, as such, tralokinumab has not been approved for utilization in children/adolescents (<18 years of age), nor is it recommended for pregnant women.6

Supporting Evidence from Clinical Trials (Figures 1-5)

Results from Pivotal Phase 3 Monotherapy Studies

In a phase 3 multicenter, randomized, double-blind, placebo-controlled clinical trial of adult patients (n=802) with moderate-to-severe AD (ECZTRA 1), the efficacy and safety of tralokinumab 300 mg SC Q2W (n=603) versus placebo (n=199) was evaluated.8 At week 16: the primary endpoint of an Investigator Global Assessment (IGA) score of clear or almost clear (IGA 0/1) was achieved by 15.8% and 7.1% of patients treated with tralokinumab and placebo, respectively (p<0.002) (Figure 1); an improvement of ≥75% and ≥90% in the Eczema Area and Severity Index (EASI75 and EASI90, respectively) was achieved by 25.0% and 14.5% of patients treated with tralokinumab versus 12.7% and 4.1% of patients treated with placebo (p<0.001 and p<0.05, respectively) (Figure 2); pruritus Numerical Rating Scale (NRS) improved by 20.0% with tralokinumab versus 10.3% with placebo (p=0.002); and there was a reduction in Dermatology Life Quality Index (DLQI) scores by 7.1 with tralokinumab and 5.0 with placebo, respectively (p=0.002) (Figure 3). Safety evaluation revealed similar adverse event (AE) profiles between the tralokinumab and placebo groups, with the majority of treatment-emergent AEs (TEAEs) being mild and self-limiting in nature. The most observed TEAEs with tralokinumab included viral upper respiratory tract infection (URTI) (23.1%), conjunctivitis (10.0%), and eczema herpeticum (0.5%). One case of conjunctivitis led to treatment discontinuation. No injection-site reactions (ISRs) were observed in either treatment group.8

In another phase 3 multicenter, randomized, double-blind, placebo-controlled clinical trial of adult patients (n=794) with moderate-to-severe AD (ECZTRA 2), the efficacy and safety of tralokinumab 300 mg SC Q2W (n=593) versus placebo (n=201) was evaluated.8 At week 16: the primary endpoint of IGA 0/1 was achieved by 22.2% and 10.9% of patients treated with tralokinumab and placebo, respectively (p<0.001) (Figure 1); EASI75 and EASI90 were achieved by 33.2% and 18.3% of patients treated with tralokinumab versus 11.4% and 5.5% of patients treated with placebo (p<0.001 and p<0.05, respectively) (Figure 2); pruritus NRS improved by 25.0% with tralokinumab versus 9.5% with placebo (p<0.001); and there was a reduction in DLQI by 8.8 with tralokinumab and 4.9 with placebo, respectively (p<0.001) (Figure 3). Safety evaluation revealed similar AE profiles between the tralokinumab and placebo groups, with the majority of TEAEs being mild and self-limiting in nature. The most observed TEAEs with tralokinumab included URTI (8.3%), conjunctivitis (5.2%), and eczema herpeticum (0.3%). No cases of conjunctivitis led to discontinuation. In addition, no ISRs were observed in either treatment group.8

By week 52, IGA 0/1 responses achieved at week 16 with tralokinumab Q2W were maintained, without any rescue therapy (including TCS), by 51% (ECZTRA 1) and 59% (ECZTRA 2) of patients who continued to receive tralokinumab Q2W versus 47% (ECZTRA 1) and 25% (ECZTRA 2) of patients who were rerandomized from tralokinumab Q2W to placebo (p=0.60 and p=0.004, respectively) (Figure 4). In addition, by week 52, EASI75 responses achieved at week 16 with tralokinumab Q2W were maintained by 60% (ECZTRA 1) and 56% (ECZTRA 2) of patients who continued to receive tralokinumab Q2W versus 33% (ECZTRA 1) and 21% (ECZTRA 2) of patients who were rerandomized from tralokinumab Q2W to placebo (p=0.056 and p<0.001, respectively) (Figure 5).8 A subset of patients following week 16 were downdosed from Q2W to Q4W dosing of tralokinumab. By week 52, 39% (ECZTRA 1) and 45% (ECZTRA 2) of patients maintained their week 16 IGA 0/1 responses despite being switched from Q2W to Q4W dosing (Figure 4). In addition, by week 52, 49% (ECZTRA 1) and 51% (ECZTRA 2) of patients maintained their week 16 EASI75 responses despite being switched from Q2W to Q4W dosing (Figure 5).

Tralokinumab for Moderate-to-Severe Atopic Dermatitis in Adults - image
Figure 1. Summary of short-term IGA responses (IGA 0/1 with at least 2-grade improvement in baseline IGA score) at week 16 for tralokinumab from pivotal phase 3 clinical trials8,9
aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline; IGA, Investigator Global Assessment; PBO, placebo; Q2W, every 2 weeks; TCS, topical corticosteroid; TRALO, tralokinumab.
Figure 2. Summary of short-term EASI75 and EASI90 responses at week 16 for tralokinumab from pivotal phase 3 clinical trials8-10
aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline; EASI, Eczema Area and Severity Index; Q2W, every 2 weeks; Q4W, every 4 weeks; TCS, topical corticosteroid
Figure 3. Summary of patient-reported outcomes (DLQI and Pruritus NRS) for tralokinumab from pivotal phase 2 and 3 clinical trials8-10,12
aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline;
cChange in mean DLQI (point reduction) and pruritus NRS (% improvement) from baseline
Figure 4. Summary of long-term IGA responses (IGA 0/1 with at least 2-grade improvement in baseline IGA score) at week 32 and week 52 for tralokinumab from pivotal phase 3 clinical trials8-10
aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline
cPatients received Q2W until week 16, then Q4W after week 16
Figure 5. Summary of long-term EASI 75 responses at week 26, week 32, and week 52 for tralokinumab from pivotal phase 3 clinical trials8-10
aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline;
cPatients received Q2W until week 16, then Q4W after week 16

Results from Pivotal Phase 3 Combination Therapy Studies

In a phase 3 multicenter, randomized, double-blind, placebo-controlled clinical trial of adult patients (n=380) with moderate-to-severe AD (ECZTRA 3), the efficacy and safety of tralokinumab 300 mg SC Q2W + TCS (n=253) versus placebo + TCS (n=127) was evaluated. The TCS utilized was mometasone furoate 0.1% cream. At week 16: the primary endpoint of IGA 0/1 was achieved by 38.9% and 26.2% of patients treated with tralokinumab + TCS and placebo + TCS, respectively (p=0.015) (Figure 1); EASI75 and EASI90 were achieved by 56.0% and 32.9% of patients treated with tralokinumab + TCS versus 35.7% and 21.4% of patients treated with placebo + TCS (p<0.001 and p<0.022, respectively) (Figure 2); pruritus NRS improved by 45.5% with tralokinumab + TCS versus 34.1% with placebo + TCS (p=0.037); and there was a reduction in DLQI by 11.7 with tralokinumab + TCS and 8.8 with placebo + TCS, respectively (p<0.001) (Figure 3). By week 32, in patients receiving tralokinumab Q2W + TCS, 89.6% and 92.5% maintained their week 16 IGA 0/1 and EASI75 responses, respectively (Figure 4 and 5, respectively). A subset of patients following week 16 were downdosed from tralokinumab Q2W to Q4W dosing. At week 32, 77.6% and 90.8% of patients maintained their week 16 IGA 0/1 and EASI75 responses, respectively, despite being switched from Q2W to Q4W dosing (Figure 4 and 5, respectively).9 Safety evaluation revealed similar AE profiles between the tralokinumab + TCS and placebo + TCS groups, with the majority of TEAEs being non-serious and self-limiting in nature. The most observed TEAEs with tralokinumab + TCS included URTI (19.4%), conjunctivitis (13.1%), and eczema herpeticum (0.4%). Six patients permanently discontinued treatment with tralokinumab due to non-serious AEs, one of which was conjunctivitis.9 No ISRs were observed in either treatment group.

In another phase 3 multicenter, parallel, randomized, double-blind, placebo-controlled clinical trial of adult patients (n=277) with moderate-to-severe AD (ECZTRA 7), the efficacy and safety of tralokinumab 300 mg SC Q2W + TCS (n=140) versus placebo + TCS (n=137) was evaluated. The TCS utilized was mometasone furoate 0.1% cream.10 At week 16: the primary endpoint of EASI75 was achieved by 64.2% and 50.5% of patients treated with tralokinumab + TCS and placebo + TCS, respectively (p=0.018) (Figure 2); EASI90 was achieved by 41.1% of patients treated with tralokinumab + TCS versus 29.3% of patients treated with placebo + TCS (p<0.001) (Figure 2); pruritus NRS was reduced by 4 with tralokinumab + TCS versus 3.1 with placebo + TCS (p<0.001); and there was a reduction in DLQI by 11.2 with tralokinumab + TCS and 9.6 with placebo + TCS, respectively (p=0.009) (Figure 3). By week 26, in patients receiving tralokinumab + TCS, 68.8% achieved EASI75 and 48.6% achieved EASI90, compared with 55.3% and 36.4% for placebo + TCS (p=0.014 and p=0.027, respectively) (Figure 5). Safety evaluation once again showed similar AE profiles between the tralokinumab and placebo groups, with the majority of TEAEs being non-serious and self-limiting in nature. The most observed TEAEs with tralokinumab included URTI (26.8%), conjunctivitis (9.4%), and eczema herpeticum (0.7%). One patient permanently discontinued treatment with tralokinumab due to an AE that was not deemed serious.10 No ISRs were observed in either treatment group.

Summary of Results from Pivotal Phase 3 Monotherapy and Combination Therapy Study Results and Additional Analyses

In summary, tralokinumab was more effective than placebo in both monotherapy and combination therapy studies, with tralokinumab demonstrating greater efficacy than placebo for patients with moderate-to-severe AD across all phase 3 clinical trials. Interestingly, rates of eczema herpeticum were higher in the placebo groups as opposed to the tralokinumab groups.8-10 An additional pooled analysis (n=1605) of five completed double-blind, randomized, placebo-controlled, phase 2 and 3 clinical trials of tralokinumab in adult patients with moderateto- severe AD examined the rates of conjunctivitis within these studies; it was found that tralokinumab had a slightly higher incidence of conjunctivitis (7.5%) in comparison to placebo (3.2%), with the majority of cases being mild-to-moderate in severity and 75% of events resolving before the treatment period was over in both groups.11

Tralokinumab was also shown to have a significant impact on health-related QoL in a phase 2b randomized, double-blind, placebo-controlled clinical trial involving adult patients (n=204) with moderate-to-severe AD. At week 6, a 5.4-point reduction in DLQI was observed with tralokinumab monotherapy, while a 2.3-point reduction in DLQI was observed with placebo (p=0.05). At week 16, a 6.8-point reduction in DLQI was observed with tralokinumab monotherapy, while a 3.5-point reduction in DLQI was observed with placebo (p=0.006) (Figure 3).12

Tralokinumab may also help resolve other IL-13-associated skin abnormalities. In a phase 2 randomized, double-blind, placebo-controlled study (n=204), adult patients with moderate-to-severe AD treated with tralokinumab had lower rates of Staphylococcus aureus colonization, fewer skin infections requiring systemic antimicrobial therapy, and a lower frequency of eczema herpeticum when compared to placebo groups.7 In another phase 2, 30-week, double-blind, randomized, placebo-controlled clinical trial (n=215), it was shown that tralokinumab did not impair vaccine-induced immune responses in adult patients receiving tetanus-diphtheria-pertussis (Tdap) or meningococcal vaccines.13

Special Populations

Tralokinumab has not been approved for utilization in children/ adolescents (<18 years of age), although a phase 3, multicenter, randomized, double-blind, placebo-controlled, parallel-group clinical trial in adolescent patients (12-17 years of age) with moderate-to-severe AD is still ongoing.14 Tralokinumab is currently not recommended in pregnant or breastfeeding women. It remains unknown if the drug is excreted in breast milk. There were no differences in terms of efficacy or safety with use in elderly patients (≥65 years of age).6

Table 1. Summary of the efficacy and quality of life data for tralokinumab from pivotal phase 2 and 3 clinical trials in adult patients with moderate-to-severe AD

Placebo + TCS

Week 6

Study 112

Tralokinumab (300 mg Q2W) Placebo P-value
Change in mean DLQI from baseline 5.4-point reduction 2.3-point reduction p=0.05
Week 12

Study 112

Tralokinumab (300 mg Q2W) Placebo P-value
Change in mean DLQI from baseline 6.8-point reduction 3.5-point reduction p=0.006
PHASE 3: Short-term efficacy and QOL data
Week 16

Study 1 (ECZTRA 1)8

Tralokinumab (300 mg Q2W) Placebo P-value
Proportion of patients achieving IGA 0/1 15.8% 7.1% p<0.002
Proportion of patients achieving EASI75 25.0% 12.7% p<0.001
Proportion of patients achieving EASI90 14.5% 4.1% p<0.05
Change in mean DLQI from baseline 7.1-point reduction 5.0-point reduction p=0.002
Percent change in mean pruritus NRS from baseline 20.0% improvement 10.3% improvement p=0.002

Study 2 (ECZTRA 2)8

Tralokinumab (300 mg Q2W) Placebo P-value
Proportion of patients achieving IGA 0/1 22.2% 10.9% p<0.001
Proportion of patients achieving EASI75 33.2% 11.4% p<0.001
Proportion of patients achieving EASI90 18.3% 5.5% p<0.05
Change in mean DLQI from baseline 8.8-point reduction 4.9-point reduction p<0.001
Percent change in mean pruritus NRS from baseline 25.0% improvement 9.5% improvement p<0.001

Study 3 (ECZTRA 3)9

Tralokinumab (300 mg Q2W) + TCS Placebo + TCS P-value
Proportion of patients achieving IGA 0/1 from baseline 38.9% 26.2% p=0.015
Proportion of patients achieving EASI75 56.0% 35.7% p<0.001
Proportion of patients achieving EASI90 32.9% 21.4% p=0.022
Change in mean DLQI from baseline 11.7-point reduction 8.8-point reduction p<0.001
Percent change in mean pruritus NRS from baseline 45.4% improvement 34.1% improvement p=0.037

Study 4 (ECZTRA 7)10

Tralokinumab (300 mg Q2W) + TCS Placebo + TCS P-value
Proportion of patients achieving EASI75 64.2% 50.5% p=0.018
Proportion of patients achieving EASI90 41.1% 29.3% p=0.032
Change in mean DLQI from baseline 11.2-point reduction 9.6-point reduction p=0.009
Change in mean pruritus NRS from baseline 4.0-point reduction 3.1-point reduction p<0.001
PHASE 3: Long-term efficacy data
Week 52

Study 1 (ECZTRA 1)8

Tralokinumab (300 mg Q2W)

Tralokinumab (300 mg Q2W to Q4W)c

Placebo P-value
Proportion of patients maintaining IGA 0/1 response achieved at week 16 51.0% 39.0% 47.0% p=0.60
Proportion of patients maintaining EASI75 response achieved at week 16 60.0% 49.0% 33.0% p=0.056

Study 2 (ECZTRA 2)8

Tralokinumab (300 mg Q2W)

Tralokinumab (300 mg Q2W to Q4W)c

Placebo P-value
Proportion of patients maintaining IGA 0/1 response achieved at week 16 59.0% 45.0% 25.0% p=0.004
Proportion of patients maintaining EASI75 response achieved at week 16 56.0% 51.0% 21.0% p<0.001
Week 32

Study 3 (ECZTRA 3)9

Tralokinumab (300 mg Q2W) + TCS

Tralokinumab (300 mg Q2W to Q4W) + TCSc

Placebo + TCS P-value
Proportion of patients maintaining IGA 0/1 response achieved at week 16 89.6% 77.6% NR NR
Proportion of patients maintaining EASI75 response achieved at week 16 92.5% 90.8% NR NR
Week 26

Study 4 (ECZTRA 7)10

Tralokinumab (300 mg Q2W) + TCS Placebo + TCS P-value
Proportion of patients achieving EASI75 response achieved at week 16 68.8% 55.3% p=0.014
Proportion of patients achieving EASI90 response achieved at week 16 48.6% 36.4% p=0.027

Table 1. Summary of the efficacy and quality of life data for tralokinumab from pivotal phase 2 and 3 clinical trials in adult patients with moderate-to-severe ADa,b

aAll studies included used non-responder imputation (NRI) statistical method of data analysis;
bAll patients received a 600 mg SC loading dose at baseline;
cPatients received Q2W until week 16, then Q4W after week 16;
AD, atopic dermatitis; BSA, body surface area; DLQI, Dermatology Life Quality Index; IGA, Investigator Global Assessment; NR, not reported; Q2W, every 2 weeks; Q4W, every 4 weeks; TCS, topical corticosteroid

Counselling: Practical Tips to Optimize Administration

Tralokinumab is administered as an SC injection. Optimal anatomic sites for the SC injection include the lower limb (specifically thigh) or trunk (specifically abdomen, excluding a 5 cm radius around the navel); the upper limb (specifically lateral upper arm) may also be used if another individual can administer the medication. Multiple doses should be delivered in the same anatomic site but at different points within that anatomic site. Doses should be rotated to different anatomic sites with each subsequent set of SC injections. Tralokinumab should not be injected into tender or damaged skin. If a patient and/or a caregiver wishes to administer the SC injection, proper training should be provided. If a dose is missed, the missed dose should be administered as soon as possible and the scheduled dosing regimen continued.6

Conclusion

Tralokinumab is an effective and safe treatment for adult patients with moderate-to-severe AD. It may be used alone or in combination with TCS. This biologic can be considered first-line treatment after failure of or intolerance to topical therapies, and, as such, represents an important tool in our therapeutic armamentarium.

References



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