Kbi-110 Access
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Report: KBI‑110 – Technical, Commercial, and Strategic Overview
(Prepared: 11 April 2026)
| Phase | Design | Population | Primary Endpoint | Status | |---|---|---|---|---| | Phase I (2022‑23) | Randomized, single & multiple ascending dose, 56 healthy volunteers | Safety, PK/PD, JAK1 biomarker (pSTAT1) | • MTD not reached • Linear PK up to 30 mg | Completed – favorable safety & PK | | Phase IIa (2023‑24) | Open‑label, dose‑ranging (5‑30 mg QD), 84 psoriasis pts | PASI‑75 at week 12 | 5 mg PASI‑75 28 % → 30 mg PASI‑75 64 % | Data published (J Dermatol Ther 2025) | | Phase IIb (2025‑26) NCT05874231 | 210 pts, 3:1 randomization (30 mg vs placebo) | PASI‑90 at week 16 (key) | 30 mg achieved PASI‑90 in 48 % vs 6 % placebo (p<0.001) | Ongoing – DSMB recommended progression to Phase III | | Phase III (planned 2027‑28) | Global, 4‑arm (30 mg, 15 mg, active comparator, placebo) | PASI‑100 at week 16; HRQoL (DLQI) | Target: ≥ 30 % PASI‑100 (30 mg) | Protocol finalized; IND amendment submitted Aug 2026 |
BRD9 is a member of the SWI/SNF chromatin‑remodeling complex. In the past five years, high‑throughput CRISPR screens have linked BRD9 hyper‑activity to: KBI-110
| Disease Context | Evidence | |----------------|----------| | Acute Myeloid Leukemia (AML) | Dependency on BRD9 for survival of certain AML sub‑types (Nat. Chem. Biol., 2020). | | Idiopathic Pulmonary Fibrosis (IPF) | Up‑regulation of BRD9‑driven pro‑fibrotic transcriptional programs (JCI Insight, 2022). | | Neurodegeneration | BRD9‑mediated microglial activation contributes to neuroinflammation in mouse models of ALS (Cell Reports, 2023). |
Because BRD9 sits at the intersection of epigenetic regulation, inflammation, and cellular stress, it became an alluring “high‑value” target for KBI’s drug‑discovery platform.
| Disease | Current Standard | Unmet Need | How KBI‑110 Could Help | |---------|------------------|------------|------------------------| | AML (MLL‑rearranged) | Cytarabine‑based chemotherapy, venetoclax + azacitidine | High relapse rates, drug‑resistance driven by epigenetic plasticity | Targeted epigenetic brake that spares normal hematopoiesis; oral administration reduces hospital burden | | IPF | Nintedanib, pirfenidone (both with GI & hepatic toxicity) | Limited efficacy; progressive fibrosis despite therapy | Directly dampens BRD9‑driven fibrotic transcription; potential for combination with anti‑fibrotic agents | | ALS | Riluzole, edaravone (modest survival benefit) | No disease‑modifying therapy; neuroinflammation a key driver | Microglial BRD9 inhibition may curb chronic neuroinflammation without broad immunosuppression | However, if you’re interested in a different kind
If the clinical trajectory follows the pre‑clinical promise, KBI‑110 could become one of the first therapeutics to modulate a SWI/SNF component with an oral small‑molecule, opening a new therapeutic class.
| Attribute | KBI‑110 | Tofacitinib | Bimekizumab | |---|---|---|---| | Administration | Oral QD | Oral BID | SC q4w | | Key Safety Advantage | JAK1‑selective → < 2 % anemia, neutropenia | JAK1/3 → 8‑10 % anemia, ↑ infection risk | Injection‑site reactions, candidiasis | | Efficacy (PASI‑90) | 48 % (Phase IIb) | 35 % (Phase III) | 57 % (Phase III) | | Time to PASI‑75 | 8 weeks | 12 weeks | 4 weeks | | Pricing (US) | Projected $2,400/yr (generic‑style) | $4,800/yr | $30,000/yr (mAb) | | Market Share Opportunity | 12‑15 % of oral segment (≈ $500 M) by 2029 | Stable | Limited (biologic niche) |
| Year | R&D Spend | SG&A | Net Revenue | EBITDA | |---|---|---|---|---| | 2026 (pre‑launch) | $120 M | $45 M | $0 | –$165 M | | 2027 (launch) | $80 M | $70 M | $210 M | –$‑ | | 2028 | $45 M | $85 M | $620 M | $395 M | | 2029 | $30 M | $95 M | $1.2 B | $1.0 B | | 2030 | $25 M | $100 M | $1.4 B | $1.3 B | | Phase | Design | Population | Primary
Assumptions: 30 % market penetration in the oral segment by 2029, 5‑year peak sales $1.4 B, 15 % CAGR post‑peak, tax rate 21 %.
KBI’s chemistry team screened >1.5 million compounds in a fluorescence‑polarization bromodomain binding assay. The top hit, a tricyclic hetero‑aryl scaffold (code‑named KBI‑001), displayed sub‑micromolar affinity (KD ≈ 300 nM) but suffered from poor pharmacokinetics.
Iterative structure‑guided medicinal chemistry (leveraging co‑crystal structures of BRD9‑KBI‑001) led to a series of C‑terminal linker modifications that improved both potency and metabolic stability. The fifth generation, bearing a pyridyl‑urea moiety and a tetrahydro‑isoquinoline side chain, emerged as KBI‑110. Its key properties are summarized below:
| Property | Value | |----------|-------| | BRD9 binding KD | 12 nM (biophysical SPR) | | Selectivity | > 200‑fold vs. BRD4, BRD7, and other BET bromodomains | | Oral bioavailability (rat) | 62 % | | Half‑life (mouse) | 7 h (plasma) | | CNS penetration | 0.8 × plasma (unbound) | | Safety window (in vitro) | No cytotoxicity up to 30 µM in primary hepatocytes |