CDT Increases Stake in Sarborg following its Quantum Computing and Intellectual Property Expansion

CDT Boosts Sarborg Stake Amid Quantum Computing and IP Growth

CDT Equity Inc. announced a strategic transaction to increase its equity stake in Sarborg Limited to 22.7%. This was achieved through the issuance of pre-funded warrants to purchase up to 12,131,770 shares of CDT's common stock, pending shareholder approval on August 28, 2026. The increased investment reflects Sarborg's significant progress, including the expansion of its Signature Intelligence platform into quantum computing with SarborgQ, and broadening its technological reach beyond pharmaceuticals into agriculture. Sarborg has also developed a growing intellectual property portfolio, including new applications in cystic fibrosis and rare disease signature matches. A previous funding round valued Sarborg at approximately $638.3 million.

• CDT Equity Inc. has strategically increased its equity stake in Sarborg Limited to 22.7% through the issuance of pre-funded warrants for up to 12,131,770 shares of CDT's common stock. This transaction, subject to shareholder approval on August 28, 2026, strengthens CDT's strategic alignment with Sarborg, building on an initial acquisition made in February 2026, and is expected to create long-term value for CDT shareholders.
• Sarborg has significantly expanded its Signature Intelligence platform, notably by launching SarborgQ, a dedicated quantum computing division. This division applies quantum-assisted coformer selection to accelerate intellectual property generation across its asset portfolio. Furthermore, Sarborg has broadened its technology's reach beyond pharmaceuticals into agricultural applications, exemplified by a recent patent filing for field-deployable combination interventions for sugarcane, and published its PRISM cross-species signature mapping framework.
• Sarborg has continued to build a robust portfolio of intellectual property assets spanning both the pharmaceutical and technology sectors. This includes new applications specifically targeting the cystic fibrosis market and the identification of novel biological targets and rare disease signature matches utilizing its proprietary disease signature databases. The platform, originally focused on pharmaceutical asset evaluation, now extends its commercial reach across agriculture, animal health, and other industrial applications.

Sarborg's AI Uncovers Novel Targets in Cystic Fibrosis

Recent research is expanding the CF therapeutic landscape well beyond established CFTR modulators, moving toward genotype-agnostic curative strategies, precision-based functional testing, and novel antimicrobial approaches for persistent Pseudomonas aeruginosa infections. These emerging directions aim to address unmet needs in patients with rare CFTR variants, pancreatic dysfunction, and chronic sinonasal disease.

• Genotype-agnostic curative approaches: Gene and mRNA therapies are being explored as universal treatments for all people with CF, representing a shift away from mutation-specific strategies and offering promise for patients regardless of underlying genotype.

• Precision and functional precision medicine (FPM): For patients with genotypes ineligible for CFTR modulators, FPM strategies use patient-derived organoids (PDOs) to functionally test treatment responses, bridging the gap between genomic data and phenotypic complexity, and offering a means to predict individual treatment efficacy.

• Expanded modulator use in rare variants: Elexacaftor/tezacaftor/ivacaftor (ETI) is being investigated in patients with rare CFTR variants (e.g., W1282X) not traditionally eligible for modulator therapy, with reported FEV1% improvement of 12% (72% to 84%), sweat chloride reduction (83 mEq/L to 9 mEq/L), and enhanced exercise capacity after one month—despite limited organoid responsiveness in some cases.

• Pancreatic function reversal with ETI: Beyond pulmonary benefits, ETI is being studied for its potential to reverse pancreatic insufficiency. Among 24 individuals with paired pre- and post-ETI fecal elastase values, 8.3% converted to moderate sufficiency and 12.5% to pancreatic sufficiency, with earlier initiation age (median 5.28 years) correlated with better outcomes and a mean conversion time of ~11 months.

• Phage tail-like bacteriocins (PTLBs) for P. aeruginosa: As an alternative to phage therapy, PTLBs (tailocins) are being explored as resistance-resilient antimicrobials, given their bacteriophage-like tail structure without genetic material. Screening of 75 P. aeruginosa genomes identified 34 distinct PTLBs, including 11 novel F-type subtypes; among these, R1 and F15 PTLBs demonstrated the strongest in vitro efficacy and achieved >75% survival in the Galleria mellonella in vivo infection model.

• Biologics for CF-related upper airway disease: Dupixent (dupilumab) is being evaluated for CF-related chronic rhinosinusitis with nasal polyposis (CRSwNP), showing statistically significant improvement in SNOT-22 scores at 6 months (V = 21, p = 0.031) comparable to non-CF populations, though nasal polyp score improvements did not reach statistical significance—relevant given the mixed type-2 endotypes common in CF-associated CRSwNP.

• Imaging biomarkers for modulator response monitoring: Low-dose and ultra-low-dose lung CT protocols (effective doses of 2.4 and 0.56 mSv) are emerging as sensitive tools for short-term monitoring of CFTR modulator therapy, capturing substantial reductions in mucous plugging (73%) and bronchial wall thickening (51%) following Trikafta® initiation.

Evolving Cystic Fibrosis Landscape: Where Sarborg's IP Fits

The cystic fibrosis treatment paradigm has undergone a fundamental transformation over the past five years, driven predominantly by the widespread adoption of elexacaftor/tezacaftor/ivacaftor (ETI, Trikafta/Kaftrio). Uptake surged from just 2% in 2019 to 71% by 2024, expanding highly effective modulator therapy (HEMT) eligibility to approximately 90% of the CF population following its 2019 approval—a marked leap from ivacaftor's 2011 debut, which covered only 4% of patients. Pivotal trial data demonstrate the magnitude of this shift: ETI produced an 11.2 percentage point improvement in ppFEV1 and a 42.8 mmol/L greater reduction in sweat chloride versus tezacaftor/ivacaftor at 24 weeks, with parallel gains in CFQ-R respiratory scores (15.9-point treatment difference). These benefits have proven durable and extend across age groups, including pediatric cohorts (ages 6–11 and adolescents), where FEV1 z-scores, FVC, and MMEF 25/75 all improved significantly alongside meaningful reductions in sweat chloride and BMI-for-age gains. Population-level European registry data corroborate these trial findings, showing mean ppFEV1 rising from 66.1% to 78.8% between 2014 and 2024, with most gains concentrated after 2020, alongside a near-doubling of adults over 30 and a 45% increase in the adult CF population share.

Beyond pulmonary endpoints, ETI's systemic effects are reshaping the broader clinical picture of CF as a chronic, multisystem disease rather than a primarily respiratory one. Nutritional and hepatic improvements are consistent across studies, with increased weight, BMI, and albumin suggesting enhanced nutrient absorption, while renal CFTR function is partially restored, reducing risks of electrolyte disturbances. However, this metabolic normalization carries a complex trade-off: cholesterol, triglycerides, apolipoprotein-B, and adipokine levels rise post-ETI, with dysregulated leptin-adiponectin relationships signaling potential cardiovascular risk even as inflammatory markers improve. This heterogeneity—improved chronic inflammation alongside worsened lipid profiles—alongside an aging CF population now experiencing increased malignancy and metabolic complications, is prompting a recalibration of long-term monitoring strategies and de-escalation of adjunctive symptomatic therapies, which recent data suggest can be achieved safely without compromising lung function outcomes. Notably, real-world implementation data from France indicate that treatment optimization remains imperfect, with only 75–79% of patients achieving optimal implementation at one to two years, underscoring persistent adherence and access challenges even amid transformative efficacy.

For pipeline strategy, the emergence of next-generation modulators signals where unmet need and competitive differentiation will concentrate. Vanzacaftor-tezacaftor-deutivacaftor, a once-daily regimen currently in phase 3 development, has shown ppFEV1 improvements of 14.2–15.9 percentage points and sweat chloride reductions exceeding 45 mmol/L in phase 2 trials—outcomes that appear competitive with ETI while offering dosing convenience. Meanwhile, approximately 10% of people with CF carry variants unresponsive to current modulators, and exploratory work on alternative potentiators (e.g., genistein, Cact-A1) combined with elexacaftor/tezacaftor points toward incremental efficacy gains for difficult-to-treat genotypes. Biomarker research, particularly MMP9 downregulation via the NF-κB pathway as a marker of therapeutic response, offers a potential tool for stratifying responders. Against this backdrop of near-saturated modulator uptake in eligible populations, the strategic opportunity lies in addressing the residual 10% with non-responsive variants, optimizing real-world implementation and adherence, and developing complementary therapies targeting the emerging metabolic and cardiovascular sequelae of long-term HEMT exposure—precisely the white space where Sarborg's IP is positioned to contribute.

Addressing Unmet Needs in Cystic Fibrosis Treatment

While the advent of highly effective modulator therapy (HEMT) has revolutionized care for many individuals with cystic fibrosis (CF), significant challenges and limitations persist in the current treatment landscape. Addressing these unmet needs is critical for improving outcomes across the entire CF population, including those who do not benefit from existing modulators and those facing complex treatment regimens.

• Limited Applicability and Efficacy: Approximately 10% of people with CF have genetic variants that are not amenable to any approved CFTR modulator. Furthermore, a significant number of individuals are unresponsive to these drugs, leaving a substantial portion of the patient population without a highly effective therapeutic option.

• Barriers to Access: The substantial cost of HEMT poses a major barrier to treatment, limiting its global accessibility and creating significant health inequity issues for patients who cannot afford these life-changing therapies.

• Uncertain Long-Term Safety and Efficacy: The treatment effect of CFTR modulators is considered suspensive rather than curative, and their long-term efficacy and safety have not yet been fully assessed. More research is needed to understand potential long-term adverse effects, drug-drug interactions, impacts on pregnancy, and effects on extra-pulmonary manifestations.

• Treatment Burden and Adherence: As new therapeutics are developed, the complexity and burden of care for CF patients increases, leading to challenges with treatment adherence. There is a need for comparative effectiveness research and novel technologies to reduce this burden while maintaining therapeutic efficacy.

• Off-Target Effects: Although generally well-tolerated, CFTR modulator use can be complicated by off-target effects. These include hepatotoxicity, clinically significant drug-drug interactions, and putative mental health issues that require careful monitoring and management.

• Suboptimal Management of Comorbidities: Gaps remain in the evidence-based management of common comorbidities such as cystic fibrosis-related diabetes (CFRD). While insulin therapy is widely used, its correlation with lung function improvements is not well-established, and robust clinical trials are needed to assess the efficacy of various glucose-lowering medications in this population.