New Developments in the Treatment of Moderate-to-severe Psoriasis: Biologics

Based on the Maui Derm 2018 presentation by Craig L. Leonardi, MD, Associate Clinical Professor of Dermatology, St. Louis University Medical School, St. Louis, Missouri

Article by Jo Ann LeQuang and the Journal of Clinical and Aesthetic Dermatology

Cytokines, those small proteins that regulate specific activities of a wide range of immunocompetent cells, are only beginning to be elucidated. Their main known function can be described, perhaps simplistically, as regulating the communication among cells within and outside of the immune system. It is quite possible that not all cytokines have been discovered, but recent advances have identified several and their in-vivo functions. The main groups of cytokines are the pro-inflammatory/anti-inflammatory cytokines (described here), cytokines related to neutrophil and eosinophil recruitment and activation, Th cell cytokines, T-regulatory (Treg) cell cytokines, and cytokines involved in the recruitment and growth of T-cells. Signaling pathways within the nucleus and cytoplasm of the cell connect cytokine receptors; these pathways can activate cytokines (along with other factors) during or after transcription.98,99

Cytokines appear to be the main mediators of the cutaneous inflammation associated with psoriasis.100 The cytokine network is extremely complex: cytokines can change the expression of receptors which, in turn, can change how responsive a source and/or target cell are to the cytokine. In treating psoriasis, targeting specific cytokines for inhibition has reduced chronic inflammation and led to major advances in controlling the disease. The main families of cytokines associated with psoriasis are TNF alpha, IL, and TGF beta.101 Humanized monoclonal antibodies (the -mab suffix drugs) target specific cytokines, and some have shown promise in the treatment of psoriasis. The cytokines associated with psoriasis appear in Figure 1, many of which have become important new targets for drug development.102

Figure 1. The cytokines associated with psoriasis ranging from the most pro-inflammatory (far left) the most anti-inflammatory (far right)

Certolizumab-pegol. Certolizumab-pegol (CZP) is a monoclonal antibody that targets TNF alpha. It is a PEGylated antigen-binding fragment (Fab) of a humanized TNF-inhibitor monoclonal antibody. CZP has been approved for use by the FDA for the indications of Crohn’s diseases (2008), rheumatoid arthritis (2009), active psoriatic arthritis (2013), ankylosing spondylitis (2013), and most recently for the treatment of psoriasis.103 The CIMPASI-1 (n=234) and CIMPASI-2 (n=227) placebo-controlled trials104 evaluated SQ CZP in patients with moderate-to-severe plaque psoriasis, scored based on the PASI and PGA scores, and found significant improvements in both active groups versus placebo at 16 weeks. In CIMPASI-2, patients were randomized to one of three treatment arms: 400mg SQ CZP every two weeks (n=87), 400mg SQ CZP at Weeks 0, 2, and 4 followed by 200mg every two weeks thereafter for 16 weeks (n=91), and placebo every two weeks (n=49). The primary endpoint of the study was meeting PASI75 at 16 weeks, which was achieved by 82.6 percent of the first group (400mg every 2 weeks), 81.4 percent of the second group (400/200mg), and 11.6 percent of placebo patients. The PGA endpoint called for improvement of at least two points by 16 weeks; 71.6 percent, 66.8 percent, and 2.0 percent met this endpoint in the first, second, and placebo groups, respectively. Thus, CZP demonstrated significant improvements from baseline at 16 weeks compared with placebo for both PASI75 and PGA endpoints. Adverse events were similar to those reported when using CZP for other approved indications.104,105

Guselkumab. Guselkumab is an IL23-P19 inhibitor and was evaluated in a 48-week, Phase III, double-blind, placebo-controlled VOYAGE 1 trial.106 Patients were randomized into one of three groups: 1) patients (n=329) received guselkumab 100mg (Weeks 0 and 4 and then every 8 weeks), 2) patients (n=174) started with placebo at Weeks 0, 4, and 12 and then rotated to guselkumab at Weeks 16 and 20 and every eight weeks thereafter, and 3) patients (n=334) received adalimumab 80mg at Week 0, 40mg at Week 1, then 40mg every two weeks through Week 47. Endpoints were the PASI score, the patient-reported outcomes on the Dermatology Life Quality Index, and the Psoriasis Symptoms and Signs Diary. Guselkumab demonstrated significant superiority (p<0.001) to placebo at 16 weeks (85.1% vs. 6.9% on Investigator Global Assessment Score [IGA]) and 73.3 percent versus 2.9 percent showed a 90-percent or greater improvement in PASI score over baseline. When compared to adalimumab, guselkumab was significantly superior (p<0.001) in IGA and PASI90 at Weeks 16, 24, and 48.106 During the placebo-controlled phase of the study, at least one adverse event was reported by 49.4 percent, 51.7 percent, and 51.1 percent of the placebo, guselkumab, and adalimumab groups, respectively; over the entire course of the study, 73.9 percent of the guselkumab group and 74.5 percent of adalimumab group reported at least one adverse event. In the group that transitioned from placebo to guselkumab, 64.8 percent of patients reported at least one adverse event during Weeks 16 to 48. Serious adverse events were reported by less than five percent of all patients; 4.9 percent of guselkumab and 4.5 percent of adalimumab patients reported at least one serious adverse event over the course of the study.106 In a Phase II study of guselkumab, ACR 20/50/70 scores showed the significant superiority of guselkumab over placebo. 107

Tildrakizumab. Like guselkumab, tildrakizumab targets IL-23 p19 and was shown in two Phase III clinical trials to be more effective than placebo and etanercept for treating moderate-to-severe plaque psoriasis.108 In these international multicenter, three-part, parallel-group, randomized, double-blind studies, patients were randomized to tildrakizumab 200mg, tildrakizumab 100mg, or placebo (reSURFACE-1 N=1,772) or to tildrakizumab 200mg, tildrakizumab 100mg, placebo, or etanercept 50mg (reSURFACE-2 , N=1,090). In the reSURFACE-1 study, at Week 12, 192 patients (62%) in the 200mg group and 197 patients (64%) in the 100mg group achieved PASI75, compared with nine patients (6%) in the placebo group. In the reSURFACE-2 study, at Week 12, 206 patients (66%) in the 200mg group, and 188 patients (61%) in the 100mg group achieved PASI75, compared with nine patients (6%) in the placebo group and 151 patients (48%) in the etanercept group. Serious adverse events were similar and low in all groups in both of these trials. One patient died in reSURFACE-2 (tildrakizumab 100mg group) but the cause of death could not be determined. The FDA approved tildrakizumab for market release in March 2018 for the treatment of plaque psoriasis.

Risankizumab. Risankizumab targets IL-23 p19, and the IMMhance trial evaluated its use against placebo over 16 weeks, but results are not yet published. From data on file at AbbVie, preliminary results found that 73.2 percent of risankizumab patients achieved PASI90 and 47.2 percent PASI100 at 16 weeks compared with 2.0 percent and 1.0 percent for placebo, respectively. In a recent study of 166 patients with moderate-to-severe plaque psoriasis,92 patients were randomized to receive subcutaneous risankizumab (one 18mg dose at Week 0 or 90 or 180mg doses at Weeks 0, 4, and 16, or ustekinumab (45mg or 90mg based on body weight at Weeks 0, 4, and 16). At Week 12, of the patients who had a 90-percent or greater reduction in their PASI score, 77 percent were in the risankizumab group (pooled 90mg and 180mg group results) versus 40 percent in the ustekinumab group (p<0.001). Results demonstrated durability up to 20 weeks for risankizumab. A serious adverse event was reported by 12 percent of patients in the risankizumab 18mg group, 15 percent in the risankizumab 90mg group, and eight percent ustekinumab, including one MACE and two BCCs. No serious adverse events were reported in the risankizumab 180mg group.92

Mirikizumab. A relatively new monoclonal antibody to be evaluated for the treatment of moderate-to-severe plaque psoriasis is mirikizumab, which targets IL-23 p19. A Phase II randomized, multicenter, double-blind, placebo-controlled trial is being conducted using different doses of mirikizumab and evaluating them for safety and efficacy is ongoing [ Identifier: NCT02899988]. Results of this study were presented at the 2018 American Academy of Dermatology Annual Meeting [Abstract # 6131] by Rich et al. In this study, 205 patients were randomized to mirikizumab 300mg every eight weeks (Q8W), 100mg Q8W, 30mg Q8W, or placebo Q8W over the course of 16 weeks. The mirikizumab 300mg and 100mg groups were significantly more likely to achieve PASI90 at 16 weeks compared to placebo (67% and 59%, respectively vs. 0 in placebo, p<0.001). Twenty-nine percent of the mirikizumab 30mg group achieved PASI90 at 16 weeks, but this was not significant compared to placebo. PASI100 scores were achieved by significantly more patients in the mirikizumab 300mg and 100mg groups than the placebo group at 16 weeks (31%, p=0.007 for both); 16 percent of the patients in the mirikizumab 30mg group achieved PASI100 at 16 weeks, which was significant versus placebo (0%, p=0.039). Pooling safety results from all mirikizumab groups, at least one TEAE was reported by 48.4 percent of mirikizumab patients compared with 48.1 percent of the placebo patients, and 1.3 percent of the mirikizumab patients and 1.9 percent of the placebo patients reported at least one serious adverse event.

Secukinumab. The IL-17 family of cytokines includes IL-17A, IL-17A/F, IL-17F, IL-17E, and IL-17C, and secukinumab targets IL-17A. There are long-term data for secukinumab showing that five-year PASI score improvements are durable over time.109 At Year 1, 168 patients entered the extension study, and at the end of Year 5, 126 patients completed 300mg (every 4 weeks) treatment. PASI 75/90/100 responses at Year 1 (88.9%, 68.5% and 43.8%, respectively) were sustained to Year 5 (88.5%, 66.4% and 41%, respectively). Results from Future 5, a placebo-controlled study, evaluated 300mg and 150mg of secukinumab and 150mg secukinumab with no loading dose compared with placebo,89 and in this study, significantly more patients achieved PASI75 and PASI90 with secukinumab compared to placebo.

Ixekizumab. Ixekizumab targets IL-17A, and the UNCOVER-3 trial provides long-term data with durable efficacy up through 108 weeks. In this randomized, controlled, Phase III study, 1,346 patients with moderate-to-severe plaque psoriasis were randomized to one of four treatment arms.110 Patients received ixekizumab 80mg every two or four weeks, etanercept 50mg twice a week, or placebo. Patients entered the long-term extension phase at Week 12 when all patients were switched to ixekizumab every four weeks.

The results of a head-to-head comparison of ixekizumab compared to ustekinumab111 reported that 52.2 percent more patients in the ixekizumab group achieved PASI100 scores at 52 weeks compared to those in the ustekinumab group (35.5%).

Brodalumab. In contrast to ixekizumab, which binds to IL-17, brodalumab binds to the IL-17 receptor and, in that way, prevents IL-17 from activating that receptor. In two Phase II studies comparing brodalumab to ustekinumab in patients with moderate-to-severe plaque psoriasis, brodalumab was associated with significant clinical improvements compared to ustekinumab.112 At 12 weeks, brodalumab 210mg resulted in 44 percent of patients achieving PASI100 scores compared with 22 percent of the patients taking ustekinumab in AMAGINE-2; these results were similar to AMAGINE-3, where 37 percent of patients in the brodalumab group achieved PASI100 scores compared to 19 percent of patients in the ustekinumab group (p<0.001, both). Rates of neutropenia were higher with brodalumab and ustekinumab versus placebo. Safety issues with brodalumab surfaced around this time when a numeric imbalance was noted in terms of cases of depression, suicidal ideation, and suicidal behavior. During the Phase III brodalumab trials, the manufacturer introduced psychological surveys to help detect patients at risk but the intervention was not successful. All trials were halted in the second quarter of 2015, but brodalumab was eventually approved by the FDA in 2017 with a black box warning.113 It should be noted in this context that, overall, patients with psoriasis appear to have higher rates of suicidal ideation than the general population. A 1993 survey found that 5.5 percent of patients with psoriasis had active suicidal ideation at the time of the study, and the more severe the patient considered his or her psoriasis, the more likely the patient was to have suicidal thoughts.114

Bimekizumab. Bimekizumab has a novel dual mechanism of action in that it neutralizes both IL-17A and IL-17F, two key pro-inflammatory cytokines.115 Based on clinical data on file with UCB, in the Phase II BE ABLE clinical study, 79 percent and 60 percent of bimekizumab patients achieved PASI90 and PASI100 scores, respectively, in 12 weeks. The safety and efficacy of bimekizumab was demonstrated in a first-in-human randomized clinical trial assessing patients with mild plaque psoriasis.116 Based on early results, this new agent appears to hold promise for the treatment of psoriasis.

The paradigm shift and future directions. The classic treatment of psoriasis had always been a stepwise progression from over-the-counter products to prescription topicals to phototherapy and then, if these treatments were no longer effective, finally to systemic therapy. In all cases, patients were expected to receive treatment in an orderly sequence, step by step, and not skip any steps. Aggressive therapy was reserved only for those patients who failed more conservative approaches. Today, the evolution of new drugs for psoriasis and the increased understanding of its pathogenesis have resulted in our discarding the classic paradigm in favor of a new approach. If a patient with psoriasis is an appropriate candidate for topical treatment, that should be the first-line approach; if that fails or the patient is not a good candidate for topical therapy, then there are three main types of therapy: biologic agents, traditional systemic agents (such as methotrexate), and phototherapy. The choice of therapy must be based on the individual characteristics of the patient. Within each group there are further therapeutic choices, again based on the needs of the individual patient. There is no longer any need for a patient to have to progress through and fail multiple treatment steps before receiving biologic therapy.


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106. Blauvelt A, Papp KA, Griffiths CE, et al. Efficacy and safety of guselkumab, an anti-interleukin-23 monoclonal antibody, compared with adalimumab for the continuous treatment of patients with moderate to severe psoriasis: results from the phase III, double-blinded, placebo- and active comparator-controlled VOYAGE 1 trial. J Am Acad Dermatol. 2017;76(3):405–417.

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109. Bissonnette R, Luger T, Thaci D, et al. Secukinumab demonstrates high sustained efficacy and a favourable safety profile in patients with moderate-tosevere psoriasis through 5 years of treatment (SCULPTURE Extension Study). J Eur Acad Dermatol Venereol. 2018;32(9):1507–1514.

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Update on the Pathogenesis of Psoriasis: A Bench-to-Bedside Success Story

Based on the Maui Derm 2018 presentation by Andrew Blauvelt, MD, MBA, Oregon Medical Research Center, Portland, Oregon

Article by Jo Ann LeQuang and the Journal of Clinical and Aesthetic Dermatology

Psoriasis is caused by the complex interplay of four factors: autoantigens, environmental antigens, genetics, and the immune system. Autoinflammation, an inflammatory state not mediated by circulating autoantibodies and autoreactive T-cells, has recently been implicated as well.65 Genetics remains the key to better understanding the immune system and the pathogeneses of all autoimmune disorders, including psoriasis. Better understanding of the pathogenesis of psoriasis will allow for more accurate mapping of psoriasis pathways and improved ability to identify therapeutic targets, which, in turn, will lead to safer and more effective treatments.

The genetics of psoriasis. Psoriasis has strong heritability, and over 70 susceptibility loci/genes associated with psoriasis have been identified to date.66 In monozygotic twins, there is approximately a 70-percent genetic concordance, and 10 percent of the children of parents with psoriasis will develop psoriasis themselves (a 4- to 5-fold increase over general population). In the 1970s, psoriasis was found to be associated with the HLA Class I antigens, with associations between psoriasis and HLA-C (HLA-Cw6 in particular) and HLA-B alleles.67 The most common and dominant gene association is HLA-C*0602, but only 41 percent of people with psoriasis are HLA-C*0602-positive.68 In fact, the HLA-C*0602 gene, in and of itself, is neither necessary nor sufficient to develop psoriasis. About 20 percent of the population are carriers of the HLA-C*0602 gene, and about 10 percent of carriers develop psoriasis.66

Autoantigens. Antigens are molecules that induce an immune response in a host organism, and antibodies are the body’s method to target these antigens. Antigens are typically peptides, polysaccharides, and lipids that originate endogenously or exogenously. Autoantigens are endogenous antigens that are produced by normal cell metabolism or as a result of a viral or bacterial infection. The major histocompatibility (MHC) Class I antigen pathway serves to alert the immune system of the presence of a cell with a viral infection. MHC molecules are expressed on nucleated cells and platelets. In humans, HLA-A, HLA-B, and HLA-C correspond to MHC Class I, while HLA-DP, HLA-DM, HLA-DOA, HLA-DOB, HLA-DQ, and HLA-DR correspond to MHC Class II. Thus, autoantigens are endogenous proteins that can be attacked by the immune system, which is the reason they are associated with autoimmune disorders.

HLA-C*0602 is an MHC Class I molecule that normally presents autoantigens to CD8 T-cells. The autoantigens are ADAMTSL5 and LL-37. ADAMTSL5 is a peptide derived from the protein ADAMTSL5 and produced by melanocytes that can bind to HLA-C*0602 and stimulate psoriatic CD8+ T-cells. LL-37 is an antimicrobial peptide produced by keratinocytes, and it contains a VRSRRCLRL-like peptide that stimulates psoriatic T-cells.66

Environmental antigens also play a role in psoriasis. Streptococcal M proteins contain peptides that overlap with hyperproliferative keratin (K16/K17) peptides; these Streptococcal M proteins can stimulate psoriatic T-cells and have been implicated in certain cases of guttate psoriasis as environmental antigens. Yeast proteins are known to contain a VRSRRCLRL-like peptide that can stimulate psoriatic T-cells, and these exogenous antigens have been implicated in cases of beer-exacerbated psoriasis.66

The psoriasis pathways: targets and mechanisms of actions. Psoriasis can be defined as a T-cell-mediated disease mainly driven by pathogenic T-cells that produce high levels IL-17 in response to IL-23. Greater understanding of the IL-23/T-17 axis, identified as the main pathway for psoriasis, has revolutionized the way psoriasis is treated today by offering important targets for pharmacotherapeutic interventions.69 Broadly blocking this pathway (e.g., with methotrexate) might work, but it might not be as safe or effective as a narrower blockade (e.g., TNF inhibition), which targets inflammation more specifically and results in greater efficacy and greater patient safety. However, if the target could be even more narrowly considered—that is, targeting psoriatic inflammation specifically along the IL-23, IL-17A, and IL17RA pathways—this should, in theory at least, allow for even greater safety and better effectiveness. Selective IL-23 blockers include guselkumab, tildrakizumab, and risankizumab. Selective IL-17A blockers include secukinumab, ixekizumab, and bimeizumab. Brodalumab blocks IL-17RA. Thus, pharmacological targets can be viewed as a continuum, with IL-23 the most upstream target and IL-22 and IL-17A downstream. While all of these points represent pharmacologically sound therapeutic targets, there are clinical differences among the inhibitors for these targets (Table 3).69,70


Not all of the cells that produce IL-17A are regulated by IL-23. Some cells, like Th17, depend on IL-23 in order to produce IL-17A, but others produce IL-17A independently of IL-23. This means that IL-23 inhibition will affect some IL-17A producers (those that depend on IL-23) but not the IL-23-independent IL-17A producers. Furthermore, it is thought that some of the IL-17A produced by cells other than Th17 in the skin and the gut might protect the body from candidiasis and inflammatory bowel disease. This would explain the association of candidiasis and inflammatory bowel disorder with IL-17 but not IL-23.69

As a general rule, the pharmacodynamic effects of a drug greatly exceed its pharmacokinetic effects, with the result being that a drug might have an impact on the underlying disease long after it has been eliminated from the body. For example, IL-23 inhibition might also cause the death of pathogenic skin-resident memory T17 cells, which depend on IL-23 for survival. Thus, the prolonged drug effect in destroying these T17 cells might lead to more durable psoriasis control.69

In a study evaluating clinically resolved psoriatic lesions,71 it was found that the lesions contained psoriasis-specific IL-17-producing alpha beta T-cell clones. Healed psoriatic skin (treated with phototherapy and etanercept) showed oligoclonal populations of T-cells, which produce IL-17. This observation might explain why new psoriatic lesions tend to recur at the same site as healed lesions.71


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67. Chandran V. Genetics of psoriasis and psoriatic arthritis. Indian J Dermatol 2010;55(2):151–156.

68. Okada Y, Han B, Tsoi L, et al. Fine mapping of major histocompatibility complex associations in psoriasis and its clinical subtypes. Am J Hum Genet. 2014 Aug 7;95(2):162–72.

69. Hawkes JE, Chan TC, Krueger JG. Psoriasis pathogenesis and the development of novel targeted immune therapies. J Allergy Clin Immunol. 2017;140(3):645–653

70. Maxwell JR, Zhang Y, Brown WA, et al. Differential roles for interleukin-23 and interleukin-17 in intestinal immunoregulation. Immunity. 2015;43(4):739–750.

71. Matos TR, O’Malley JT, Lowry EL, et al. Clinically resolved psoriatic lesions contain psoriasis-specific IL-17-producing alphabeta T cell clones. J Clin Invest. 2017;127(11):4031–4041.