Investment case

Avacta is a clinical-stage UK-based life sciences company developing exquisitely targeted therapies for cancer, enabled by its proprietary pre|CISION technology platform. pre|CISION is a highly specific substrate for a tumour associated enzyme (fibroblast activation protein, FAP) which, when conjugated to a cytotoxic drug, can be used to improve efficacy, reduce systemic toxicities, and optimise dosing. Lead asset faridoxorubicin (FAP-Dox, AVA6000), a pre|CISION doxorubicin conjugate, has completed Phase Ia, demonstrating proof of concept for the platform and is the precursor to a next-generation pipeline of pre|CISION-enabled peptide-drug conjugates (PDCs). These include AVA6103 (FAP-EXd) and AVA6207 (a novel first-in-class dual payload PDC). Avacta listed on AIM in 2006, with in-licensing of pre|CISION from Tufts University in 2018 creating the current business. Since 2022, Avacta has raised c £66.5m (gross) in equity with a further £55m via a five-year convertible bond (£20.4m principal outstanding at end-October 2025). Avacta employs c 20 FTEs and is headquartered in White City, London (UK).

Valuation

Our risk-adjusted NPV (net present value) valuation includes disclosed pipeline assets plus an indicative placeholder valuation for the pre|CISION platform. The rNPVs are summed and netted against unallocated operating costs and net cash. Our faridoxorubicin rNPV is blended, comprising an orphan opportunity which Avacta could potentially commercialise alone and a larger commercial opportunity where a partner is likely needed. Given there are few details on AVA6103 and AVA6207, these are currently placeholder valuations. Our updated rNPV based valuation is £468m ($585m), equivalent to 106p/share (92p/share fully diluted).

Financials

End-June 2025 cash of £12.6m together with the October 2025 £16m (gross) fundraise should provide a cash runway into H226. This allows management to progress its clinical programmes through to the next inflection points. These include Phase I initiation for second asset AVA6103 (FAP-EXd) in Q126, Phase I faridoxorubicin data in triple negative breast cancer (TNBC) during H126, and further details on the recently disclosed dual payload peptide drug conjugate programme AVA6207.

Sensitivities

Avacta is now a therapeutics business and, in common with most innovative drug development companies, the main sensitivities relate to clinical trial outcomes, navigating regulatory hurdles, ensuring timely and sufficient financing, concluding partnering discussions successfully and, eventually, gaining attractive pricing and reimbursement, and executing commercial plans. Financing is a perennial industry-wide issue and positive clinical data will be key to attracting equity funding and/or commercial deals, which are necessary to fund and progress the wider pipeline. 

Avacta: Targeting cancer with pre|CISION

Avacta’s investment case centres on its proprietary pre|CISION drug delivery platform, which aims to reduce the efficacy/safety trade off seen with many potent therapeutics, thus expanding their reach. The pre|CISION platform is being harnessed to develop novel, highly targeted cancer drugs, and has been validated by lead programme faridoxorubicin (AVA6000, FAP-Dox), a peptide-drug conjugate (PDC) of doxorubicin. Early clinical data for faridoxorubicin have shown selective activation at the target tumour site, resulting in lower toxicities than standard doxorubicin, and improved tolerability. Phase I data has informed the design of the registrational study in salivary gland cancer (SGC), an orphan indication, with potential for parallel development in triple negative breast cancer (TNBC) which will deliver first clinical data in H126. Phase I initiation of second pre|CISION asset AVA6103 (FAP-EXd), a novel sustained release PDC with an exatecan payload, is on track for Q126 with initial data due in Q426. Further disclosures on dual payload PDC AVA6207 are also expected by year-end. These clinical and pipeline catalysts should provide multiple near-term value inflection points, with indication-specific clinical proof of concept data key to unlocking partnerships. Our Avacta valuation is £468m, or 106p/share.

Avacta’s focus is on exploiting the full potential of its proprietary pipeline and pre|CISION platform. Its long-term aim is to develop and commercialise a broad pipeline of peptide-drug conjugates (PDCs) that use its pre|CISION technology to improve the therapeutic index of many highly potent yet systemically toxic oncology drugs, allowing their targeted delivery and cleavage in the tumour microenvironment (TME) by FAPα (fibroblast activation protein-α), a tumour-associated enzyme expressed by cancer associated fibroblasts (CAFs).

Continued successful clinical progress with faridoxorubicin has provided proof of concept, helping validate the pre|CISION technology and its FAP-activated drug release mechanism of action, positioning it for Phase II development with a future partner. Progressing the current pipeline and securing sustainable funding for this is a priority for Avacta. The cash runway extends into Q326, beyond several potential pipeline catalysts; however, additional resources are required to fully fund the next stage of faridoxorubicin clinical development and to move the next wave of assets (AVA6103, AVA6207) into and through the clinic.

During 2025 Avacta concluded various initiatives to increase its appeal to global specialist healthcare investors (ie removal of the convertible bond repayment overhang, diagnostic division divestment, and further insights into earlier stage programmes). In addition, business development to secure product partnerships or technology collaborations to accelerate development/commercialisation and to exploit more fully the wide-ranging opportunities that could be addressed with pre|CISION technology is ongoing. New pre|CISION chemistry and IP related to capping groups (to tune pharmacokinetics) and novel linkers (to effect sustained payload release or enable dual payloads) has expanded the platform potential to encompass new payloads and broader cancer types, while potentially addressing limitations of antibody-drug conjugates. This, plus first clinical data for AVA6103, should interest potential partners and new investors, establishing pre|CISION as a viable and valuable platform, and positioning FAP-EXd (pre|CISION-enabled exatecan PDC) as a proven payload, including for dual payload PDCs.

Building value with a pre|CISION pipeline

Avacta’s proprietary pipeline assets are all enabled by its pre|CISION technology platform which allows the delivery of potent therapeutics (‘payloads’) specifically to the tumour microenvironment (TME) where they remain inert until activation by FAP-cleavage. This means that systemic exposure of these toxic cancer drugs is minimised, allowing optimisation of dosing (eg higher or more frequent dosing) and/or the therapeutic window for otherwise highly potent drugs with tolerability issues, with the goal of improving patient outcomes.

Our November 2024 Outlook provided a detailed overview of the pre|CISION technology, how it differs from other FAP-targeting approaches (in short, the pre|CISION peptide is a substrate for the FAP enzyme, rather than antigen binding target), and how computational chemistry is used to design pre|CISION molecules and to fine tune their components to achieve the desired therapeutic profile.

The current pipeline (Exhibit 1) includes lead programme faridoxorubicin (AVA6000, FAP-Dox) a doxorubicin PDC; AVA6103 (FAP-EXd), a Phase I-ready sustained release PDC targeting topoisomerase I (Topo I) via an exatecan payload; and AVA6207, the first in a novel class of engineered biotherapeutics – dual payload PDCs. Avacta’s pipeline should deliver meaningful news flow over the next 12 months, with key catalysts including: (1) initial faridoxorubicin Phase I data in TNBC in H126, and start of Phase II trials in SGC and TNBC planned for 2026 (subject to partnership or funding); (2) Phase Ia initiation for AVA6103 (following FDA IND clearance) in Q126 and potential for first data in Q426, before embarking on Phase Ib expansion cohorts in early-2027; and (3) nomination of the first dual payload pre|CISION PDC product candidate (AVA6207) during H226.

Exhibit 1: Avacta’s therapeutic pipeline

Source: Avacta

Faridoxorubicin Phase I data to date have contributed to a better understanding of FAP biology as well as supporting the further clinical development of this asset and, importantly, providing proof of concept for the pre|CISION technology. The data demonstrated targeted doxorubicin release in the TME, improved safety and tolerability vs standard doxorubicin with no dose-limiting toxicities nor cardiac safety signal, and preliminary signs of efficacy in high grade soft tissue sarcomas and SGC. Further data is due this year and will help inform Phase II development, most likely with a partner. Achievement of clinical proof of concept in TNBC should support business development discussions.

pre|CISION chemistry unlocks broader opportunities

The pre|CISION platform is very flexible and can be used to create a variety of highly tailored therapeutic conjugates with specific characteristics. Faridoxorubicin is a relatively simple pre|CISION PDC, with the FAP-cleavable peptide attached directly to doxorubicin. However, second- and third-generation PDC formats employ more advanced chemistry to confer additional advantages, expanding the applicability of the pre|CISION technology to a wider range of payloads and more extensive range of cancer indications, while potentially also addressing many of the limitations of antibody-drug conjugates (ADCs). These advances in chemistry are covered by new foundational IP and patents (Exhibit 2) and give advantages such as the ability to:

• tune the pharmacokinetic profile with alternative capping groups – this alters the physical properties of the PDC and/or released payload allowing for a longer plasma half-life and ensuring longer retention or sustained release of the payload in the TME;
• effect sustained payload release with additional linkers – inserting self-immolative linkers between the payload and pre|CISION peptide adjusts the release kinetics of the FAP enzyme; and
• enable PDCs to carry a dual payload with novel linkers – allowing simultaneous delivery of two complementary payloads to the TME to enhance tumour killing.

Exhibit 2: Three IP families align with the product pipeline

Source: Avacta

While the chemistry of pre|CISION peptides lends itself to delivering a variety of different payload types, both of Avacta’s earlier-stage disclosed programmes (AVA6103 and AVA6207) incorporate exatecan, the most potent Topo I inhibitor to be evaluated in the clinic (albeit subsequently discontinued due to tolerability issues and a short half-life). We note that Enhertu (trastuzumab deruxtecan), AstraZeneca/Daiichi Sankyo’s tumour-agnostic HER2-directed ADC mainly used for breast cancer, is based on an exatecan derivative and generated $3.4bn of revenue in 2024. Thus, if AVA6103 can achieve clinical proof of concept and validate the promising preclinical results generated to date, this, coupled with considerable commercial potential, could make it an attractive licensing candidate.

Management is encouraged by translational data which shows that the sustained release of exatecan by AVA6103 demonstrates optimal tumour to plasma concentration in xenograft models vs comparative data for doxorubicin release by faridoxorubicin (Exhibit 3), especially since the doxorubicin tumour to plasma  ratio was further enhanced in Phase I patients vs animal models.

Exhibit 3: Tumour to plasma concentrations by FAP-EXd vs FAP-Dox

Source: Avacta

The next step for AVA6103 is the anticipated start of the Phase Ia basket study in Q126. Avacta, in collaboration with Tempus AI, has queried the latter’s extensive real world datasets of diverse tumour samples and clinical data from over 200k patients to identify the addressable patient populations for AVA6103. Four FAP-positive cancer indications (cervical, gastric, pancreatic, and small cell lung cancer) have been selected for clinical evaluation on the basis that SLFN11 co-expression is a predictor of sensitivity to Topo I inhibition. A similar approach will be applied to de-risk future pre|CISION-enabled programmes.

Partnerships could help advance pipeline

Partnering is a central part of Avacta’s strategy to fully exploit the potential of its pre|CISION platform through both advancing and expanding its pipeline. Out-licensing opportunities exist for later-stage development and commercialisation of proprietary assets (with faridoxorubicin likely the nearest-term prospect) as well as collaboration deals to create innovative next-generation cancer therapeutics by combining the pre|CISION technology with novel payloads. The focus is on prioritising and moving forward the most commercially promising and relevant assets; hence, AVA6207 (dual payload PDCs) has usurped AVA7100 (pre|CISION biologic-drug conjugates) as Avacta’s third programme, due in part to the cost, speed, and manufacturing benefits of small molecules vs biologics, but also the potential versatility of the dual payload linker in enabling new therapeutic combinations in a single PDC.

Management intends to optimise the economics, and timing, of any potential co-development or licensing deal for its assets. We understand that multiple conversations are ongoing, and achievement of clinical proof of concept in a given indication will be a critical hurdle. Deal drivers for large pharma include the perennial search for replacement revenues for key products approaching patent expiry, but also the pursuit of a competitive edge.

Avacta’s pre|CISION PDCs could be a credible alternative to ADCs (antibody-drug conjugates), which have become established anticancer therapeutics, with 19 approved globally, and are currently a hot space in biotech with numerous M&A deals having completed. Competition appears to be mounting to achieve best-in-class status for established targets (via access to enabling technologies) or to secure first-in-class assets. Notable transactions include Daiichi Sankyo’s global ex-Japan co-development co-commercialisation collaborations with AstraZeneca (Enhertu for up to $6.9bn and Datroway for up to $6bn) and an up to $22bn deal with Merck & Co for three potentially first-in-class deruxtecan ADC programmes (based on an exatecan derivative); Pfizer’s $43bn acquisition of ADC pioneer Seagen and AbbVie’s $10.1bn acquisition of ImmunoGen. Smaller, but still significant deals include Lonza’s acquisition of Synaffix for access to enabling technologies that form the basis of multiple licensing deals with other partners.

pre|CISION’s edge over ADCs

ADCs are a three-component system (potent cytotoxic, stable linker, targeting mAb) that delivers a highly potent cytotoxic agent to tumour cells. They have a unique mechanism of action that combines targeted therapy (via mAbs binding to specific tumour-associated cell surface markers) with chemotherapy (via small molecules). PDCs have a similar mechanism of action, but unlike ADCs, they are not impacted by the same limitations (Exhibit 4). Additionally, should they reach the market, PDCs also have potential health economics benefits over ADCs, due to cheaper and quicker manufacturing (the manufacture of the mAb component is the most expensive and time-consuming part of the ADC process). Other beneficial cost considerations apply to dual payload PDCs, where combining complementary (potentially synergistic) mechanisms in one molecule requires a shorter and cheaper development pathway than a similar combination approach (where activity of both components as monotherapy and in combination needs to be demonstrated).

Exhibit 4: pre|CISION PDC platform addresses challenges in the ADC field

Source: Avacta   Note: PDC – peptide drug conjugate; DAR – drug to antibody ratio; PDR – peptide to drug ratio; IHC – immunohistochemistry

Alongside the above considerations, a key feature of pre|CISION PDCs (and not consistently possible with ADCs) is their ability to leverage the tumour specificity of FAP via the bystander effect. FAP is selectively found in a membrane-bound form on the surface of cancer associated fibroblasts (CAFs) which comprise a large portion of the tumour stroma, an important component of the TME. As FAP is necessary for the extracellular release of the payload into TME (following pre|CISION PDC cleavage), the payload becomes concentrated here where it can exploit the bystander effect to kill both FAP-positive CAFs and neighbouring FAP-negative tumour cells (Exhibit 5).

Exhibit 5: The pre|CISION bystander effect

Source: Avacta

Translational studies have confirmed payload release even at low levels of FAP expression; hence, through the bystander effect, pre|CISION PDCs could potentially be used to treat patients with low tumour FAP expression, given that it facilitates the killing of both antigen-positive and antigen-negative tumour cells. This contrasts with many other FAP-targeting approaches such as traditional ADCs (which release their payload intracellularly) or bispecific antibodies (that incorporate FAP binders) which have not worked as their impact is limited to FAP-positive CAFs, with little to no effect on tumour cells. The exception being FAP-binding peptide-targeted radiotherapy ligands (eg Novartis’ 177Lu-FAP-2286), whereby the radioligand is released in the TME and can exert its effect on both CAFs and tumour cells.

Partnering interest should rise as potential demonstrated

Acquisitions of preclinical assets for billions of dollars generate graphic headlines, but the reality is that the majority are partnered, either through licensing or development deals, and these typically happen once a body of solid clinical data have been generated. Avacta has undergone a sizeable transformation over the past 12-18 months; most obviously having now become a pure-play oncology development company rather than a diverse, and unfocussed, diagnostic business with a still nascent, and unproven, pre|CISION platform. We view the recent clinical results as being the most relevant difference. While acknowledging that it is still early data, faridoxorubicin’s efficacy in achieving tumour shrinkage essentially provides a material proof of concept and shifts the conversation from “will it work?” to “how well does it work?”.

Importantly, the new second generation and now third generation pre|CISION constructs also move the conversations from “how can we improve a proven generic treatment?” to “how can we use this platform to improve our development products?”. Certainly, the programmes being developed each have a much higher inherent partnering attractiveness in successive generation; however, we feel Avacta could evolve from an asset play into a platform-licensing play, allowing diverse partners to “pre|CISION-ise” their own proprietary payloads. If (or when) this transition was to be achieved, then Avacta’s value should be realised.

AVA6000 (FAP-Dox, faridoxorubicin)

Avacta’s lead asset, faridoxorubicin (formerly AVA6000 and FAP-Dox), is a novel pre|CISION PDC consisting of doxorubicin conjugated directly to a FAP-cleavable peptide. Clinical data from dose escalation cohorts in the Phase Ia study provide important validation for the pre|CISION platform (Exhibit 6), demonstrating tumour-specific delivery of a potent and toxic payload (doxorubicin) with minimal systemic effects, despite doses reaching nearly four times the maximum tolerated dose (MTD) of conventional doxorubicin (75mg/m²). Biopsy and plasma data collected 24 hours after administration of the first dose of FAP-Dox confirmed that the concentration of released doxorubicin payload in the tumour was dose-dependent, the median tumour to plasma ratio of released doxorubicin was 100:1, and effective cleavage of FAP-Dox leading to concentration of the payload in the tumour also occurred in low-FAP expressing tumours. This latter observation, reinforces the evidence base for the bystander effect of pre|CISION, whereby release of the payload in the TME can affect any surrounding tumour cells irrespective of whether they express FAP, and hence its potential applicability to a wider range of cancers.

Exhibit 6: Phase I FAP-Dox trial shows benefits over standard doxorubicin

Source: Avacta

Phase Ia data confirms FAP-Dox safety and early efficacy

Full Phase Ia dose escalation data for FAP-Dox was presented at the European Society of Medical Oncology (ESMO) 2025 meeting. These data, in 63 patients, confirmed a favourable safety and tolerability profile with no severe cardiac adverse events (which limits standard doxorubicin dosing) regardless of cumulative dose (the maximum dose reached was 550mg/m²). No maximum tolerated dose (MTD) was reached when FAP-Dox was dosed every three weeks (Q3W), the usual doxorubicin dosing schedule, or with more frequent fortnightly administration (Q2W), and despite dosing up to 385 mg/m² (approximately four times the conventional doxorubicin dose). The recommended dose for expansion (RDE) in the Phase Ib cohorts was 310mg/m² of FAP-Dox (equivalent to 209mg/m² conventional doxorubicin) every three weeks.

The longer-term cardiac safety data is critically important. Cardiotoxicity is a major limitation of standard doxorubicin; it is associated with a temporary or permanent reduction in left ventricular function, limits the cumulative dose that can be administered, and typically appears post therapy having a life-long impact in those patients successfully treated for their cancer. Treatment with doxorubicin is effectively limited to only six cycles (typically 60-75mg/m² every three weeks until 450mg/m² is reached). FAP-selective cleavage of FAP-Dox in the TME to release active doxorubicin means there is no systemic circulation, sparing cardiac tissue. This should allow more treatment cycles to be carried out before reaching the cumulative cardiotoxic dose, positively impacting those patients with cancers, such as metastatic breast cancer, where doxorubicin is a mainstay of treatment.

Exhibit 7: FAP-Dox Phase I trial design and patient population

Source: Avacta

Despite the Phase Ia study being designed to evaluate the safety (primary endpoint) of FAP-dox and identify the recommended dose for expansion, there was also preliminary evidence of efficacy. Several durable RECIST responses (four partial responses and five minor responses) were confirmed in patients with high grade sarcoma (a high FAP-expressing tumour type) and salivary gland cancers (SGC, where FAP expression was stromal only).

The eleven SGC patients treated at or above a FAP-dox dose of 250 mg/m² had a disease control rate (DCR) of 91%, and multiple confirmed responses (Exhibit 8). Median progression-free survival (PFS) in SGC was yet to be reached (Exhibit 9), with a 41-week median duration of PFS follow-up suggesting a durable response that is more than double the benchmark PFS (median PFS of 3.5-4 months for conventional therapy in pre-treated SGC, and 4-6.5 months in first-line SGC).

Exhibit 8: Phase Ia FAP-Dox waterfall plot of best % change in SGC patients

Source: Avacta, ESMO 2025   Note: data cut off September 15, 2025; all patients with the diagnosis of SGC treated at or above the 250 mg/m² dose level, regardless of schedule.

Exhibit 9: Phase Ia FAP-Dox swimmer plot weeks on study for SGC patients

Source: Avacta, ESMO 2025   Note: data cut off September 15, 2025; all patients with the diagnosis of SGC treated at or above the 250 mg/m² dose level, regardless of schedule.

In the 17 evaluable patients with soft tissue sarcoma (STS), stabilisation of disease despite cessation of treatment is indicative of FAP-Dox being an effective and durable treatment. Multiple tumour responses were observed (Exhibit 10), including one Partial Response at the lowest dose level evaluated: 160 mg/m² Q3W.

Exhibit 10: Phase Ia FAP-Dox waterfall plot of best % change in STS patients

Source: Avacta, ESMO 2025   Note: data cut off September 15, 2025

Phase Ib dose expansion provides consistent data

Early Phase Ia efficacy data (published at AACR 2024), the evolving competitive landscape in the respective cancer indications, and a more straightforward clinical development pathway, informed Avacta’s decision to select SGC as the orphan indication for further development ahead of STS. SGC is a chemo-refractory indication with no defined treatment regimen, whereas doxorubicin monotherapy or combination therapy is the preferred regimen for STS as stipulated by NCCN guidelines. Thus, FAP-Dox development in STS would likely require a head-to-head randomised controlled study vs doxorubicin in 1L STS, while in the 2L setting patients will already be affected by doxorubicin-related cardiotoxicity. Additionally, in 1L STS the efficacy hurdle was recently raised, with the doxorubicin comparator arm showing a longer than expected PFS of 7.9 months in Boehringer Ingelheim’s unsuccessful Phase II/III Brightline-1 trial.

Nevertheless, the ongoing Phase Ib dose expansion is enrolling patients in three indication-specific cohorts (with up to 30 patients to be enrolled in each), which were chosen based on the Phase Ia data, the unmet medical need, and their sensitivity to doxorubicin:

• Salivary gland cancer (SGC): 1L or 2L setting, any histologic subtype;
• High grade soft tissue sarcoma (HG-STS):1L/2L setting, undifferentiated pleomorphic sarcoma or dedifferentiated liposarcoma;
• Triple negative breast cancer (TNBC):1-3L setting (up to two prior lines of therapy), PD-L1-negative, BRCA wildtype.

Recently reported FAP-Dox data in SGC from both the Phase Ia (n=11) and Phase Ib (n=19) cohorts show that preliminary Phase Ib data include clinically meaningful and durable tumour shrinkage that is consistent with Phase Ia results. Baseline characteristics for patients in both cohorts were similar, with a median of one prior therapy (range of zero to two) in Phase Ib and seven of the 19 patients having received no prior systemic therapy. Across the 30 patients in both cohorts, all of whom were treated at a FAP-Dox dose of 250 mg/m² and above, the DCR was 90% with two confirmed partial responses and seven minor responses, and 25/30 patients with stable disease (Exhibit 11).

Exhibit 11: Phase Ia & Ib FAP-Dox waterfall plot of best % change in SGC

Source: Avacta   Note: Combined Phase Ia and Ib patient population in the AVA6000 trial; data cutoff 15 September 2025 (Phase Ia), 15 October 2025 (Phase Ib). All SGC patients treated at or above 250mg/m2 dose level, regardless of schedule in Phase Ia or 310mg/m2 Q3W in Phase Ib.

Exhibit 12: Phase Ib Median PFS has not been reached in SGC patients

Source: Avacta  Note: Phase Ib data cutoff 15 October 2025. ²Median Follow Up is calculated using the Reverse Kaplan Meier Method and median among 19 evaluable patients is reported

The Phase Ib data are early in the treatment course of most patients, with median PFS yet to be reached in the SGC cohort, although median follow up exceeds 15 weeks. 13/19 patients are still on treatment and an additional two patients in PFS follow up at the data cut off (Exhibit 12). This outcome measure will be critical, as PFS is highly likely to be the primary endpoint in the registrational trial. These data will continue to mature and, with enrolment ongoing (potentially up to 30 patients in total) given the favourable efficacy and clean safety profile (in the 22 patients evaluable for safety), further data updates are anticipated during H126.

Similar Phase Ib dose expansion data for the TNBC cohort (PD-L1-negative, BRCA wildtype) are also expected in H126, with this potentially providing first evidence of efficacy for FAP-Dox in TNBC as it was not an indication enrolled into the Phase Ia portion of the study. In our view, these data will further strengthen the FAP-Dox partnering package and could be a prelude to a deal. Despite its cardiotoxicity limitations (which can have lasting repercussions in successfully treated patients) and generic status, doxorubicin consistently posts >$1bn in annual global sales. Hence FAP-Dox’s clinical profile to date, showing a significant reduction in severe toxicities that limit doxorubicin dosing and in mild-to-moderate side effects that impact patient quality of life, should be attractive to potential partners that are well-positioned to fully exploit this opportunity.

FAP-Dox Phase II planned, initiation subject to funding

Further FAP-Dox development is planned in SGC and TNBC (Exhibit 13), with potential for Phase II studies to start in H126, subject to funding. Avacta’s strategy is to take a rapid route to market by targeting a first approval in an orphan indication (SGC) with an accelerated approval pathway and attractive pricing, with parallel development in TNBC to later expand the label once the pivotal Phase III reads out (Exhibit 14). First potential launch would be in 1L/2L SGC in 2028/29 assuming successful development and accelerated approval, with full approval in SGC and in 2L mTNBC occurring in a similar 2031/32 timeframe.

Exhibit 13: FAP-Dox clinical development timeline schematic

Source: Avacta

Exhibit 14: Commercial Analysis of FAP-Dox in SGC and TNBC

Source: Avacta, LEK analysis of FAP-Dox clinical development plan & commercial opportunities

SGC is a rare cancer (three cases per 100,000), representing 6-8% of all head & neck cancers, but treatment is difficult as it is typically unresponsive to chemotherapy and there is no recognised SoC (standard of care). Various treatments are employed, especially in advanced or metastatic disease where five-year survival rates are c 42%, but are hampered by limited efficacy (response rates from zero to <20%) and toxicity issues. The durable responses and meaningful PFS data seen to date with FAP-Dox, albeit in relatively small number of SGC patients, suggest that FAP-Dox could find a pivotal role in treating SGC.

TNBC is the more significant commercial opportunity given both the unmet need (representing c 15-20% of new breast cancer diagnoses, but 35% of deaths) and widespread use of doxorubicin chemotherapy (particularly in the PD-L1 negative cohort, Exhibit 15). Indications are that orphan drug pricing levels in SGC should be maintained for FAP-Dox in 2L TNBC, given that Gilead’s Trop-2-directed ADC Trodelvy (US list price of $20,106 per cycle of two infusions) is likely to move into the first line setting in TNBC following positive Phase III data.

Exhibit 15: Opportunity in metastatic triple negative breast cancer

Source: Avacta

AVA6103 (FAP-EXd): tuning pharmacokinetics

Avacta’s second pre|CISION programme, and the first of its second-generation, is AVA6103 (FAP-EXd), a FAP-enabled PDC that consists of a pre|CISION peptide linked to the highly potent Topo I inhibitor exatecan. The Topo I inhibitor mechanism of action centres on interfering with DNA replication and inducing DNA damage in cancer cells leading to cell death. AVA6103 was designed to target delivery of exatecan to the TME, using Avacta’s sustained release mechanism to take advantage of its potent efficacy profile while overcoming its limitations (severe dose-limiting toxicities, such as neutropenia and thrombocytopenia, and short half-life).

The sustained release mechanism, summarised in Exhibit 16, is a pre|CISION platform innovation achieved through altering the capping group (to extend the plasma half-life of the PDC to several hours) and the self-immolative linker (to modulate the rate of payload cleavage from the pre|CISION peptide, by adjusting the release kinetics of the FAP enzyme). Sustained release of the payload in the TME has several benefits, including very low plasma exposure to the active drug (minimising systemic toxicities through reducing peripheral exposure) and potential reduced dosing frequency (improving patient compliance) given the therapeutic effect can be exerted over a longer period.

Exhibit 16: pre|CISION platform innovation – sustained release mechanism

Source: Avacta

Pharmacological data supports sustained release MoA

Preclinical in vitro and in vivo data, both unpublished and that presented by Avacta at the April American Association of Cancer Research meeting (AACR 2025), have confirmed several important features of AVA6103:

• Highly specific delivery of exatecan directly into the TME: up to 85-fold higher levels of exatecan in tumour cells vs plasma. By contrast, and as a benchmark, in the clinic and in preclinical models, faridoxorubicin exhibited a four- to six-fold increase in the therapeutic index of doxorubicin;
• Robust and broad-spectrum antitumor activity: AVA6103 showed deeper and more durable responses than achieved with conventional exatecan in multiple patient-derived xenograft models (colorectal, gastric, pancreatic and small cell lung cancers – Exhibits 17 and 18), with biomarker analyses indicating that this resulted from on-target effects of exatecan;

Exhibit 17: Multiple durable responses with AVA6103 in PDX models of gastric cancer (left) and SCLC (right)

Source: Avacta

Exhibit 18: Consistent durable CR across a range of tumours and FAP-levels

Source: Avacta  Note: CR = complete response

• Demonstration of the bystander effect: co-culture assays showed that AVA6103 optimises the bystander effect, with released exatecan able to enter FAP-negative tumour cells following cleavage by FAP-positive cancer associated fibroblasts, resulting in the killing of both FAP-positive CAFs and FAP-negative tumour cells;
• Highly effective sustained release mechanism: compared with exatecan’s nine-hour half-life, AVA6103’s sustained release of payload extends the exposure duration of exatecan in the tumour to five days vs plasma exposure of two hours (Exhibit 19).

Exhibit 19: Tumour and plasma PK with AVA6103 show sustained release

Source: Avacta

Together, these data support the mechanism of action of sustained released pre|CISION PDC technology, and the principle behind AVA6103. GMP manufacturing and GLP toxicology are complete, the US IND is cleared, and Avacta intends to start the Phase Ia trial in Q126 with the goal of achieving clinical proof of concept in late-2026.

Exatecan: harnessing the potency of a powerful payload

Exatecan is an ideal payload for second-generation pre|CISION PDCs. The FAP-EXd PDC format of AVA6103 allows exatecan delivery to be targeted directly to tumours and activated in the TME, exploiting exatecan’s potency with a potentially lower side effect burden. Preclinical data supports this premise and the potential for AVA6103 to address multiple indications with high unmet need.

Exatecan is the most potent Topo I inhibitor to have been studied clinically (Exhibit 20), demonstrating activity in multiple solid tumours. However, due to severe dose-limiting toxicities and a short half-life (resulting in insufficient Topo I inhibition), clinical development as a monotherapy was discontinued by originator Daiichi Sankyo. Nevertheless, it has been adapted for use in other more targeted approaches, playing a central role in Daiichi Sankyo’s subsequent success as deruxtecan (DXd). DXd, an exatecan derivative, is the Topo I inhibitor payload and linker used within its blockbuster HER2-directed ADC Enhertu and the TROP2-directed ADC Datroway approved in 2025 (both partnered with AstraZeneca), as well as its earlier-stage DXd development pipeline. We note that both ADCs have boxed warnings for interstitial lung disease, a common ADC-related side effect.

Exhibit 20: Exatecan, an ideal payload for pre|CISION PDCs

Source: Avacta, Kumazawa, E. et al. Cancer ChemotherPharmacol 42, 210–220 (1998)

Defining next steps with Tempus AI insights

The broad reach of Topo I inhibitors, coupled with the prospect of longer-acting inhibition (conferred by pre|CISION chemistry) and more specific payload release reducing off-target toxicities, provides numerous potential opportunities for AVA6103. Additionally, unlike ADCs which target tumours expressing specific surface antigens (eg HER2 or TROP2), AVA6103 is tumour agnostic. The collaboration with Tempus AI has been critical in using AI to narrow down the choice of indication (and setting) to expedite and de-risk the AVA6103 clinical development plan. Avacta intends to follow a similar clinical development strategy as with faridoxorubicin, whereby development in an orphan indication with high unmet need would facilitate a rapid route to market, with parallel development in a larger patient population.

Dosing of the first patient in the Phase Ia dose escalation portion of the Phase Ia/Ib AVA6103 trial (Exhibit 21) is anticipated in Q126, with initial data in Q426; these data, in two dose escalation arms, should determine the recommended dose for expansion (RDE) and provide first clinical proof of concept for AVA6103 as well as advance partnering discussions. The Phase Ib expansion cohorts, planned to start in early-2027, will assess indication-specific safety and efficacy.

Exhibit 21: AVA6103 Phase Ia/Ib trial design

Source: Avacta

The four tumour types that will be studied in the AVA6103 Phase I include two large (pancreatic ductal carcinoma, PDAC, and gastric cancer) and two rare indications (small cell lung cancer, SCLC, and cervical cancer). They were selected based on a high likelihood of predicted response to AV6103, which was determined after querying large real-world datasets with AI to identify FAP-positive cancers with co-expression of SLNF11, a predictor for sensitivity and hence optimal responses to Topo I inhibition.

Exhibit 22: FAP and SLFN11 co-expression predicts optimal indications

Source: Avacta

AVA6207: a leap forward with dual payload PDCs

Avacta’s first-in-class dual payload PDC programme, AVA6207, is further demonstration of the versatility and broad potential of Avacta’s pre|CISION platform. This novel technology, enabled through new linker chemistry, allows a single PDC molecule to deliver two diverse and complementary therapeutic payloads simultaneously to the TME, which, following a single FAP cleavage event, can be released independently in a finely controlled manner. The kinetics of payload release are tunable, providing flexibility and allowing optimisation of the therapeutic profiles of different payload combinations, and are achieved through modifying the self-immolative linker and capping group (Exhibit 23).

Exhibit 23: pre|CISION linker design enables dual payload release

Source: Avacta

Precise details of the construct to be taken forward are not yet disclosed, but it is known that AVA6207 consists of a potent Topo I inhibitor coupled with a resistance modifying component targeting DNA repair (such as ATRi or PARP). Exatecan is the obvious toxic payload, as its properties as AVA6103 are already largely known and pre|CISION chemistry has been shown to harness its potency and diminish its off-target side effect profile.

Exhibit 24: pre|CISION platform innovation with dual payload technology

Source: Avacta

The ability to create and design a combination therapy in a single molecule could be applied to a multitude of novel combinations, potentially exploiting synergies to maximise the therapeutic effect and to also target key resistance pathways with the aim of overcoming acquired resistance to single-drug therapies. Avacta’s current dual payload PDC pipeline comprises two strategic approaches:

• combination of microtubule inhibition (MMAE, Monomethyl Auristatin E) and Topo I inhibition (exatecan), representing two distinct anti-cancer mechanisms with established clinical activity; and
• DNA damage response (DDR) agents such as inhibitors of ATR (Ataxia Telangiectasia and Rad3-related protein) or PARP (poly-ADP ribose polymerase) combined with exatecan, where inhibition of DNA damage repair (a key resistance mechanism to Topo I inhibitors) potentiates exatecan’s cytotoxic effect.

Preclinical data presented at AACR-NCI-EORTC

First preclinical data on this novel drug class was presented at AACR-NCI-EORTC Molecular Targets and Cancer Therapeutics 2025 in a poster entitled: “Discovery and characterization of novel pre|CISION technology compounds delivering complementary dual payloads to the tumour microenvironment following FAP cleavage”.

Importantly, these data validate the dual payload release mechanism, with liquid chromatography-mass spectrometry (LC-MS) analyses confirming that pre|CISION technology enables simultaneous FAP-dependent release of multiple complementary payload combinations (including FAP-EXd/MMAE, FAP-EXd/PARPi, and FAP-EXd/ATRi compounds). Notably, the bystander effect was also validated in a 3D tumour/fibroblast co-culture model which showed that with FAP-negative tumour cells, payload release was dependent on the presence of FAP-positive CAFs while limited activity occurred in the absence of these FAP-positive CAFs or with the addition of a FAP inhibitor.

Other analyses (Exhibit 25) showed potent FAP-selective tumour cell killing, with the dual payload PDCs exhibiting comparable cytotoxic activity to the free payloads in the presence of the FAP enzyme but minimal activity without FAP. Additionally, the payload delivery kinetics could be fine-tuned and optimised through modifications to the linker and capping groups.

Exhibit 25: FAP-enabled anti-tumour activity by FAP-EXd/MMAE PDCs

Source: Avacta

Importantly, data presented also confirmed that target specific biomarkers for both payloads were modulated only when FAP was present, and that both mechanisms of action were functioning as intended, which was consistent with the independent release of both payloads for FAP-EXd/MMAE (Exhibit 26) and FAP-EXd/DDRi (Exhibit 27).  Payload release from the FAP-EXd/MMAE compounds decreased TOP1 (the target protein for exatecan) as well as increasing markers for DNA damage and damage response, while tubulin depolymerisation and cell cycle arrest, characteristic of MMAE-activity, were also seen.

Exhibit 26: FAP-EXd/MMAE payload-specific biomarker modulation

Source: Avacta

Exhibit 27: FAP-EXd/DDRi payload-specific biomarker modulation

Source: Avacta

For the FAP-EXd/DDRi compounds, two formats were evaluated (Exhibit 28): FAP-EXd/PARPi (incorporating a PARP inhibitor) and FAP-EXd/ATRi (including an ATR inhibitor), both of which couple exatecan with a small molecule inhibitor that disrupts DNA repair in damaged cells.

Exhibit 28: Schematic of synergy of Topo I inhibitor with ATRi or PARPi

Source: Avacta   Note: figure generated using BioRender

Payload release from both compounds reduced TOP1 levels, with evidence of reduced PAR levels (consistent with release of the PARPi) and reduced pCHK1 (a DDR marker downstream of ATR) respectively. Alongside this, markers for DNA damage and apoptosis were elevated, including γH2AX which was synergistically increased when exatecan and PARPi were both present vs as single payloads.

As upregulation of the DDR pathway is a key resistance mechanism to Topo I inhibition, the combination of exatecan with a DDR inhibitor in a single dual payload PDC was expected to be synergistic and this has been borne out by the data. FAP-EXd/DDRi compounds demonstrated four to five-fold greater FAP-dependent tumour cell killing compared with exatecan alone (Exhibit 29), confirming the credibility of simultaneously targeting a tumour directly with a cytotoxic and overcoming potential resistance with a DDRi in a single therapeutic.

Exhibit 29: Dual payload PDCs combine a cytotoxic (exatecan) with inhibition of resistance by DDR

Source: Avacta

Next steps for AVA6207

Avacta’s goal is to complete the necessary optimisation work to enable selection of the AVA6207 development candidate in H226, at which point we would expect the identity of the DDR inhibitor payload to be confirmed. Working on a similar development timeline to AVA6103, this would suggest potential for IND filing around end-2027/early-2028. Data emerging from the AVA6103 Phase I trial over the intervening period will also inform development plans and strategy.

The platform IP underpinning the pre|CISION dual payload technology is newly developed, with anticipated patent expiry in 2045, and is an extension of Avacta’s novel linker chemistry that makes the binding and release of two active payloads from one pre|CISION molecule possible. The novelty of this approach coupled with growing industry activity and interest in dual payload ADCs, has stimulated several nascent partnering discussions on the dual payload PDC technology.

Dual targeting competitive landscape

ADCs are a fast growing and well-established class of oncology therapies, with over 200 currently in clinical development, 19 approved globally to date and several enjoying blockbuster sales. However, ADCs are not without limitations,  hence dual payload ADCs have been created to address challenges such as:

• suboptimal efficacy: often due to tumour penetration issues given the relatively large size of monoclonal antibodies (mAbs), restricting which mAbs, or which therapeutic targets, can be used;
• significant adverse effects or toxicity issues: resulting from non-specific payload release as any cell that internalises the ADC will be affected, and/or potential premature payload release into the bloodstream; as well as possible side effects caused by immune responses partially induced by antibodies to the ADC; and
• development of drug resistance: major mechanisms of resistance to ADCs include acquired payload-related resistance which likely impacts different ADCs carrying the same payload, as well as target antigen-related resistance, issues with ADC internalisation, or lysosomal dysfunction.

By combining two distinct therapeutic payloads drugs in a single targeted molecule, dual payload ADCs offer the promise of improved efficacy through synergistic effects as well as overcoming acquired resistance. A key hurdle will be clinical data that confirms the safety of this approach, particularly with respect to payload-associated toxicities, and demonstrating synergistic rather than additive efficacy and durable patient responses. However, this data will take time to materialize as while several dual payload ADCs are in preclinical development, only two companies have embarked on, or are about to start Phase I trials: Chengdu Kanghong with KH815 (a TROP2 ADC conjugated to exatecan and the RNA polymerase inhibitor triptolide) and Callio Therapeutics with CLIO-8221 (formerly HMB-802, a TROP2 targeting ADC conjugated to a TOP1 inhibitor and an ATR inhibitor payload). Other programmes expected to receive IND clearance in the near term include Crossbridge Bio’s CBB-120 (TROP2 targeting ADC plus TOP1 inhibitor and an ATR inhibitor) and two programmes from Araris/Taiho (including a triple payload candidate).

In the same way that pre|CISION PDCs have advantages over traditional ADCs in the delivery of cytotoxic payloads (eg tumour-specific delivery and release, lack of systemic toxicities, better tumour penetration, small molecule manufacturing, broader applicability) Avacta’s dual payload PDCs should also have benefits over novel dual payload ADCs. In addition to FAP-targeted payload delivery, including in patients with low tumour FAP expression though the bystander effect, the simpler small molecule manufacturing of dual payload PDCs is an important benefit. Compared with ADC manufacturing and payload conjugation, synthesis of a dual payload pre|CISION PDC is not only faster and less expensive, but lends itself to scale up, which is likely to have positive consequences for both clinical trial GMP manufacture and future commercial supply.

Sensitivities

Avacta’s strategy is now exclusively focused on developing novel therapeutics, with a pipeline of three known programmes built through the application of its proprietary pre|CISION technology. In common with most innovative healthcare companies, the three main sensitivities relate to clinical development and regulatory aspects, commercial execution, and the financial resources required to accomplish these.

Avacta is creating a pipeline of innovative oncology constructs where the key differentiator is the precise delivery of the active(s) to a tumour site. Addressing novel targets is commercially more attractive but also, clearly, carries greater risks. The pre|CISION platform’s ability to successfully target the tumour has essentially been demonstrated by the faridoxorubicin Phase I data. However, the risk profile now shifts to whether “on target, off tumour” effects may still occur. Such toxicities would typically only be noticed in larger, and later, clinical trials. While the likelihood of encountering material unexpected problems is relatively small, the impact on the commercial prospects could still be significant.

Management’s strategy envisages in-house development of smaller and orphan indications, with the larger, and more expensive indications addressed through collaborations, partnerships, and/or out-licensing. The current management has a history of successfully striking such deals and partnerships in previous roles but their ability to source, negotiate, and close appropriate deals with Avacta remains unproven. Such deals are important, not only as a source of non-dilutive funding, as they also provide useful external validation of the attractiveness of the proprietary technologies and the commercial value of the programmes.

Funding remains a perennial sensitivity for any innovative research-based company and Avacta is no exception. Cash resources currently provide funding through to H226, although additional resources will be needed to continue to progress the pipeline. The timing and means of securing sufficient funding is an important sensitivity, with others relating to:

• Progressing the pre|CISION pipeline: this includes further clinical studies of lead asset faridoxorubicin, including Phase II development in an orphan indication, as well as advancing the key PDC (AVA6103) and dual payload (AVA6207) programmes into and through clinical development; and
• Securing appropriate business development/licensing deals: these include potential deals or collaborations for the pre|CISION platform, and for the further development and/or commercialisation of known pipeline assets, particularly for larger indications that require higher investment, but also represent more lucrative opportunities.

Avacta’s sensitivities are common to all such high technology-based biotechnology and development stage companies and are well documented and understood by investors. Essentially the higher risks are accepted and are reflected in the expectations of higher potential returns. Anecdotally, after a sustained period of limited interest in the sector, investor appetite appears to be returning for attractive scientific concepts and well-run businesses.

Valuation

We value Avacta using a sum-of-the-parts model, comprising risk-adjusted NPVs (net present value) for the disclosed pipeline assets, and an indicative placeholder valuation for the pre|CISION platform. Each rNPV includes an estimate of the potential costs for each programme. The success probabilities for each are adjusted for the inherent clinical, regulatory, commercial, and execution risks. The rNPVs are summed and then netted against unallocated operating costs and net cash (excluding the convertible bond, CB, as for the purposes of our model we assume this will be settled in shares). Our valuation has been updated to incorporate the October 2025 fundraise, to include dual payload candidate AVA6207 (which replaces AVA7100), and has been rolled forwards in time. Together, these result in a small valuation uplift to £468m/$585m (from £457m), now equivalent to 106p per share based on the most recent share count (or 92p per share fully diluted including future shares to settle the CB). An overview of the key assumptions underpinning our valuation is provided in Exhibit 30.

Exhibit 30: Avacta sum of the parts valuation

Source: Trinity Delta   Note: assumptions include a 12.5% discount factor; £/$ FX rate of 1.25; * blended valuation comprising an orphan opportunity at 60% and a larger partnering opportunity at 20%

Our AVA6000 NPV is a blended valuation comprising an orphan opportunity (SGC) which Avacta could potentially commercialise alone, and a larger commercial opportunity (TNBC), where Avacta will likely need a commercial partner. We forecast total peak AVA6000 sales of $1.5bn, with c $250m for the orphan indication, and the remainder for the larger partnering opportunity. Given initial efficacy data have been reported in SGC, we assign a 60% probability to the orphan indication. For the larger partnering opportunity, we assign a lower 20% given the lack of efficacy data at present in any such indication, plus partnering execution risk, on which we have limited visibility.

We have separate valuations for each of the disclosed pipeline assets, with our assumptions for lead second-generation PDC AVA6103 unchanged, and inclusion of newly disclosed dual-payload PDC AVA6207 (replacing our valuation for AVA7100). Given the limited details on both at this stage, these remain illustrative placeholder assumptions for now:

• For AVA6103, we know that the payload exatecan has shown clinical activity in several solid tumour indications (breast, gastric, lung, and pancreatic cancers), all of which could have blockbuster potential, and that FAP-targeting is relevant in a broader array of cancers than Enhertu (which targets HER-2). Four indications have been selected for clinical development, hence our $2.5bn peak sales.
• For AVA6207, details of the construct are not yet known but the obvious toxic payload would be exatecan, as its properties as FAP-EXd are already largely known, and it would likely be coupled with a resistance modifying component targeting DNA repair, such as ATRi or PARP. We assume this could have larger potential than AVA6103 hence our $3.5bn peak sales.

As AVA6103 is the more advanced asset, we assign a 15% probability, which we acknowledge is high for a preclinical, albeit Phase I-ready programme (preclinical assets would typically have a probability <5%). However, given that AVA6000 has provided proof-of-concept for the pre|CISION platform, notably on the potential to improve safety, and that exatecan has previously demonstrated clinical activity in multiple solid tumours, we believe this is justified. For AVA6207, as this is earlier stage than AVA6103 and a development candidate has not yet been nominated, we assign a lower 7.5% probability

Our valuation also includes an indicative valuation for the pre|CISION platform. In the absence of specific details, this assumes multiple products are at various stages of preclinical development, with varying degrees of commercial potential. Avacta has previously stated that they had pre|CISION-enabled ten payloads; while we do not expect these all to enter the pipeline, there are clearly future opportunities for pipeline expansion. We highlight that the TempusAI collaboration could also offer the prospect of extensive life cycle management opportunities for pipeline programmes. We continue to attribute no material value to the AffyXell JV in our model, reflecting the current lack of visibility and early developmental stage; this non-core area could represent potential upside.

Financials

Avacta has transitioned to a pure play therapeutics business following completion of the diagnostics divestments. As such, significant and recurring revenues are unlikely in the near-term, while R&D costs are likely to rise as various products advance through clinical development. These aspects continue to be reflected in our updated forecasts, shown in Exhibit 31, which now include the October 2025 £16m (gross) fundraise. Incorporating this fundraise is the main adjustment to our last published forecasts (outlined in our October 2025 Update), with the main P&L items unchanged; the October 2025 Update also reviews interim H125 financials.

Our forecasts include token revenues in FY25 to reflect H125 trends, but nothing beyond, given the limited visibility on potential milestones or deals. Our FY25e R&D forecast of £14.8m assumes a similar level of spend in H225 to H125, and we continue to assume an uptick in FY26e to £15.5m as larger trials are initiated. Similarly for SG&A we forecast FY25e expenses of £9.3m based on the H125 trend, with an incremental increase to £9.4m in FY26e.

End-June 2025 cash and equivalents were £12.6m (vs £12.9m at end-December 2004), with a £16.9m cash balance at end-2025. In H225, Avacta completed two equity raises for a total of £6.5m gross (c £6.2m net) to fund the July and October 2025 convertible bond (CB) repayments, sold Coris for £2.15m in cash, and completed a £16m gross (we assume c £15.1m net) equity raise. This extended the cash runway into Q326, beyond key data read outs, allowing management to progress its pipeline through to the next inflection points. For the purposes of our model, we include £30m of cash inflows in FY26e (as illustrative short-term debt) to address the H226 funding shortfall. This could come from a variety of sources, such as potential licensing deals or collaborations, and debt and/or equity funding which could include the potential for dual listing on AIM and NASDAQ.

The most recent fundraise (October 2025 Lighthouse) also satisfied the terms of the CB amendments, agreed at the time of the September raise (September 2025 Lighthouse). These amendments included:

• payment of the October 2025 quarterly repayment and interest in cash;
• deferral of the January 2026 and April 2026 quarterly CB repayments and interest until October 2027; and
• the bondholder having the right to accelerate payment (in cash or shares) of one or both deferred repayments on the earlier of (i) the release of Phase Ib faridoxorubicin data in TNBC and (ii) 30 June 2026.

For the purposes of our model, the January 2026 and April 2026 repayments are deferred to October 2027, when the CB is due to be fully settled (hence we include two quarterly amortisations during H226 and six during 2027); we continue to assume that future amortisations are settled through issuing shares.
At end-June 2025, the principal balance remaining on the October 2022 £55m CB was £25.5m. Post period end, there were two quarterly amortisations of £2.55m (plus interest) in July and October; these were each settled with the £3.1m net proceeds of the July and September equity raises respectively. Consequently, the CB principal balance has been reduced to £20.4m.

Exhibit 31: Summary of financials

Source: Avacta, Trinity Delta. Note: Adjusted numbers exclude exceptionals. FY24 cash of £17.8m includes £4.9m held within Diagnostics. FY26e includes £30m cash inflow (as illustrative short-term debt) which could come from a variety of sources.

Contact details

Scale Space, White City
Imperial College Campus
58 Wood Lane
London W12 7RZ
United Kingdom

www.avacta.com

Top institutional shareholdings

Source: Avacta  Note: shareholdings correct as at March 31, 2025