[Edaily Reporter Kim Ji-wan] “Psoriasis may appear to be a skin condition, but it is actually a systemic inflammatory disease caused by an immune system disorder. We have confirmed that regulating gut microbiota can reduce skin inflammation.”

Kim Jun-hyung, Principal Researcher (Ph.D.) at GoBioLab, made these remarks while presenting research findings on the company’s microbiome-based psoriasis treatment candidate, KBL697 (Project KBLP-001), at the International Human Microbiome Consortium (IHMC 2026) recently held at COEX in Seoul.

Despite a $25 billion market, treatment limitations are clear

KBL697 is an oral microbiome therapy that utilizes live beneficial bacteria. KBL697 was initially developed as a treatment for ulcerative colitis (UC) and garnered attention as #GoBioLab’s core pipeline. However, the global Phase 2a clinical trial for ulcerative colitis was halted due to delays in patient recruitment and changes in the development strategy. Subsequently, GoBioLab pursued expanding the indications to other autoimmune diseases, such as psoriasis.

For the psoriasis indication, a global Phase 2a clinical trial was conducted in the U.S. and Australia involving 78 patients with moderate plaque psoriasis. However, in the analysis of the overall patient population, the treatment failed to demonstrate statistical significance in improving the PASI score—the primary endpoint—compared to the placebo group. Nevertheless, subgroup analyses revealed a reduction in PASI scores and lesion area in certain patient subgroups. PASI refers to an international standard assessment index that quantifies the area and severity of psoriatic lesions.

Nevertheless, this presentation at IHMC 2026 is significant in that it went beyond simply confirming efficacy to elucidating the mechanism of action. Gobao Lab confirmed the process by which strain-derived LTA activates immune regulatory pathways to alleviate psoriasis, thereby providing a basis for the further development of KBL697. Psoriasis is a chronic autoimmune disease characterized by redness, thickening of the skin, and the recurrent formation of white scales. The global patient population is estimated at approximately 125 million.

The market is also growing rapidly. According to global market research firm Fortune Business Insights, the global psoriasis treatment market was valued at approximately $29.15 billion (about 44 trillion won) last year. The market is projected to grow from $31.42 billion (approximately 48 trillion won) this year to $72.99 billion (approximately 110 trillion won) by 2034. The compound annual growth rate (CAGR) is expected to reach 11.1%. The domestic market is also estimated to be worth hundreds of billions of won.

Currently, the psoriasis treatment market is dominated by antibody therapies targeting interleukin (IL)-17 and IL-23. IL-17 is considered the most direct trigger of inflammation in psoriasis. It also acts as a kind of inflammatory “executor,” sending signals to skin cells to “proliferate faster” and “secrete more inflammatory substances.” In psoriasis patients, excessive secretion of IL-17 causes the skin to proliferate several times faster than normal, leading to the formation of erythema and scaling.

Cosentyx (active ingredient: secukinumab) is a leading treatment that directly blocks IL-17. Cosentyx has the advantage of being fast-acting and potent because it blocks signals near the final stage of inflammation. In contrast, IL-23 is an immune signaling molecule that operates at a higher level than IL-17. IL-23 plays a role in activating and sustaining the immune cells (Th17 cells) that produce IL-17. Simply put, if IL-17 is the field operative, IL-23 is more like the commander.

Tremfya (guselkumab) and Skyrizi (risankizumab) selectively block IL-23. Because they suppress inflammatory signals from the earliest stages, they are considered the most potent class of psoriasis treatments available today.

However, these treatments all share the limitation of being expensive injectable antibody therapies. They require repeated injections, and the annual treatment costs are significant. Furthermore, since IL-17 also plays a role in defending against bacterial and fungal infections, concerns have been raised that long-term suppression may increase the risk of infection.

Oral treatments such as Otzela (apremilast) and Sotictu (duclavacitinib) have also been launched. However, Otzela and Sotictu are not considered satisfactory alternatives for all patients due to side effects such as diarrhea, headaches, and nausea, as well as their limited efficacy.

“Restoring Immune Balance Rather Than Directly Blocking Inflammatory Factors”

Researcher Kim explained, “Existing treatments work by directly blocking specific inflammatory

factors

,” adding, “KBL697 is distinctive in that it restores the immune balance in the gut, which ultimately reduces inflammatory pathways such as IL-17.”

This is also why GoBioLab focused on psoriasis. While originally researching KBL697 as a treatment for inflammatory bowel disease, the research team noted that both psoriasis and inflammatory bowel disease share an IL-17-centered immune pathway.

In fact, cell and animal experiments confirmed significant therapeutic effects in psoriasis models.

When KBL697 was administered to animal models of psoriasis, skin redness, skin thickness, and scaling were markedly reduced.

In particular, compared to apremilast—currently used to treat psoriasis—and the FDA-approved TYK2 inhibitor duclavacitinib, KBL697 demonstrated similar or, under certain conditions, even superior levels of improvement.

“The Gut and Skin Are Connected”… Evidence for the Gut-Skin Axis

The research team took this a step further by investigating why KBL697 is effective. The gut-skin

axis

was identified as the key mechanism. Although the gut and skin are physically distant from each other, they are closely connected through immune cells. The concept is that immune cells activated in the gut can travel through the blood and lymphatic systems to either exacerbate or alleviate skin inflammation.

Using fluorescent labeling technology, the researchers tracked the migration pathways of immune cells originating in the gut. The results confirmed that immune cells producing IL-17—which exacerbates psoriasis—migrate to lymph nodes near the skin. In contrast, this migration was significantly reduced in animals treated with KBL697.

Another change was also observed: regulatory T cells (Tregs) increased not only in the gut but also in the lymph nodes near the skin. Regulatory T cells act as a brake on overly activated immune responses. In patients with autoimmune diseases, their function is often impaired.

In addition, levels of the anti-inflammatory cytokine IL-10 increased significantly. IL-10 is a key anti-inflammatory substance that calms excessive inflammation and inhibits tissue damage.

Researcher Kim stated, “We confirmed that immune regulation is not limited to the gut alone, but that the entire immune system connected to the skin is affected,” adding, “These results demonstrate that regulating the gut microbiota can lead to improvements in skin inflammation.”

“LTA Is the Key Switch for Efficacy”…Mechanism of Action Elucidated

One of the long-standing challenges in the field of microbiome therapeutics is the lack of clarity regarding their mechanisms of action. Even when positive effects were observed, there were many cases where researchers could not explain why those effects occurred.

The GoBioLab research team succeeded in elucidating the core mechanism of action of KBL697. After repeatedly conducting experiments involving heat treatment of the bacterial strain and protein removal to track the active ingredient, the team identified LTA (lipoteichoic acid), a cell wall component, as the key substance.

LTA stimulates the TLR2 receptor on the surface of immune cells. TLR2 acts as a sort of detection sensor that enables immune cells to recognize bacteria or foreign substances. It was found that this subsequently activates intracellular signaling pathways, increasing IL-10 production and suppressing inflammatory responses.

The research team also created a mutant strain in which the gene responsible for producing LTA was removed. As a result, the effect of increased IL-10 production disappeared, and the therapeutic effect on psoriasis was largely lost. Conversely, when the original strain was re-administered, the therapeutic effect was restored. Furthermore, LTA derived from KBL697 was found to induce IL-10 production much more strongly than the LTA produced by Staphylococcus aureus, while causing less secretion of inflammatory cytokines such as IL-6 and TNF-α.

In other words, even though it is the same LTA, the LTA from KBL697 exhibits distinct characteristics that reduce inflammation and restore immune balance.

Researcher Kim explained, “We confirmed that the therapeutic effect on psoriasis is only observed when LTA is present,” adding, “This study demonstrates that a specific component of a specific bacterial strain regulates a specific immune pathway.”

He continued, “We didn’t just stop at identifying a beneficial strain; we were able to explain exactly which substance produces the effect and through which pathway,” adding, “KBL697 has the potential to develop into a next-generation oral immunomodulatory therapy that can overcome the limitations of existing antibody therapies.”