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AVA6103

Avacta's second pre|CISION-platform peptide-drug conjugate — a fibroblast activation protein (FAP)-cleavable peptide linker masking exatecan, the topoisomerase-I payload behind the deruxtecan ADC class. First patient dosed in the Phase 1 FOCUS-01 trial (NCT07454642) on March 31, 2026, with preclinical data presented at AACR 2026.

DLimitedLimited Data
Last updated 5 citations

What is AVA6103?

AVA6103 is Avacta Therapeutics' second clinical peptide-drug conjugate (PDC) built on the pre|CISION platform. It pairs exatecan — a topoisomerase-I inhibitor and the active warhead family used in trastuzumab deruxtecan (Enhertu), datopotamab deruxtecan, patritumab deruxtecan, and ifinatamab deruxtecan — with a fibroblast activation protein alpha (FAPα)-cleavable peptide linker that masks the payload in circulation. FAPα is a serine protease highly expressed on cancer-associated fibroblasts in many solid tumors but minimally expressed in healthy adult tissue, providing a tumor-microenvironment-selective deconjugation switch. AVA6103 is described by Avacta as a 'sustained-release' PDC, distinct from the AVA6000 (FAP-doxorubicin) chemistry by virtue of a prolonged intratumoral payload-release profile. The Phase 1 FOCUS-01 trial (NCT07454642) began enrollment on March 31, 2026, targeting pancreatic ductal adenocarcinoma, cervical/vulvar, gastric/GEJ adenocarcinoma, and small-cell lung carcinoma. Preclinical data presented at AACR 2026 (abstract #5846) reported activity across low-to-high FAP-expression patient-derived xenografts, with a higher reported tumor selectivity index than a synthetic Enhertu comparator arm — a company-defined comparator, not a head-to-head trial.

What AVA6103 Is Investigated For

AVA6103 is the second clinical molecule from Avacta's pre|CISION FAP-activated PDC platform, swapping the AVA6000 doxorubicin payload for exatecan — the topoisomerase-I inhibitor whose deruxtecan derivative powers the most commercially successful ADC class in oncology. The strategic rationale is clear: exatecan provides broader tumor-type relevance than anthracyclines, a strong bystander effect for heterogeneous FAP expression, and a payload that lipophilic free exatecan could never achieve as a small molecule because of dose-limiting myelotoxicity. Preclinical AACR 2026 disclosures describe a 'sustained-release' intratumoral payload profile, faster tumor penetration, and a higher tumor selectivity index than a synthetic Enhertu comparator. Phase 1 FOCUS-01 (NCT07454642) is a 144-patient open-label dose-escalation and expansion study using BOIN methodology across Q3W and Q2W schedules. Honest caveats: AVA6103 has zero peer-reviewed publications, no human PK or efficacy data yet, and the Enhertu comparator was a synthetic arm rather than a randomized head-to-head. The FAP-activated PDC concept itself is still proving translational viability — AVA6000 reached Phase 1 in 2022–2023 with credible early activity in salivary gland cancer, but the broader FAP-PDC class has yet to deliver a registered therapy. AVA6103 should be understood as an early-stage platform-validation asset, not a near-term cancer therapy.

FAP-positive solid tumors (pancreatic, cervical/vulvar, gastric/GEJ, SCLC)
Limited15%
Tumor-selective exatecan delivery via pre|CISION linker
Limited15%
Alternative to antibody-drug conjugates in FAP-rich stroma tumors
Limited15%

History & Discovery

Avacta Therapeutics developed the pre|CISION platform as a peptide-drug-conjugate strategy in which a FAPα-cleavable peptide linker masks a cytotoxic payload in circulation and selectively releases it within the tumor stroma. AVA6000 (FAP-doxorubicin), the first clinical asset on the platform, entered Phase 1 in 2022–2023 and reported its first clinically meaningful activity signals — including durable responses in salivary gland cancer — through 2024–2026 conference presentations. AVA6103 was developed as the platform's second clinical molecule, pairing the same FAP-cleavable linker chemistry with exatecan rather than doxorubicin. The payload switch was driven by exatecan's positioning as the dominant ADC warhead class in oncology circa 2023–2026: trastuzumab deruxtecan (Enhertu), datopotamab deruxtecan, and the broader deruxtecan family of ADCs have validated the topoisomerase-I payload class commercially and clinically. By porting that payload onto the FAP-activated PDC chassis, AVA6103 aims to reach FAP-rich stromal tumors — pancreatic, cervical/vulvar, gastric/GEJ, and small-cell lung — that are less well served by current ADC target antigens. The first preclinical disclosures arrived at AACR 2026 (abstract #5846, presented April 21, 2026), describing tumor selectivity, payload concentration, and antitumor activity in multiple patient-derived xenograft models versus a synthetic Enhertu comparator arm. The Phase 1 FOCUS-01 trial (NCT07454642) opened enrollment with first patient dosed on March 31, 2026 across sites in Virginia, Texas, and Michigan, with initial human data expected later in 2026.

How It Works

Exatecan is a strong tumor-killing drug from the same family used in Enhertu (Trastuzumab deruxtecan). AVA6103 carries exatecan with a peptide 'safety lock' that only opens at tumor sites — specifically where an enzyme called FAP (fibroblast activation protein) is found on cells that surround and support tumors. The peptide gets cleaved at the tumor, releasing active drug locally with less spillover to healthy tissue.

AVA6103 is a peptide-drug conjugate consisting of exatecan linked via a FAPα-cleavable peptide bond. FAPα is a dipeptidyl-peptidase-family serine protease whose expression on cancer-associated fibroblasts is restricted to tumor stroma and sites of active fibrosis, with minimal expression in healthy adult tissues — providing the differential cleavage signal that defines the pre|CISION platform. The payload, exatecan, is a camptothecin analog roughly 10-fold more potent than SN-38 (irinotecan's active metabolite). It traps topoisomerase-I-DNA cleavage complexes, generating single-strand DNA breaks that collapse replication forks and trigger apoptosis. Exatecan as a free small molecule was abandoned in oncology development because of dose-limiting myelosuppression; payload-conjugation strategies — both ADCs (Enhertu's DXd) and now FAP-activated PDCs — were designed specifically to deliver this potency without the systemic toxicity ceiling. Avacta describes AVA6103 as a 'sustained-release' PDC, suggesting prolonged intratumoral payload availability rather than burst release. Preclinical AACR 2026 disclosures reported a tumor selectivity index roughly three-fold higher than a synthetic Enhertu comparator arm, with tumor peak concentrations more than one log greater and faster tumor penetration. These claims are sourced from a company-defined comparator within a preclinical study, not from a randomized clinical head-to-head; they should be read as platform-validation signal rather than clinical-superiority evidence.

Evidence Snapshot

Overall Confidence25%

Human Clinical Evidence

First patient treated March 31, 2026 in FOCUS-01 (NCT07454642). No human PK, safety, or efficacy data published.

Animal / Preclinical

Preliminary. AACR 2026 abstract #5846 reports activity across multiple patient-derived xenografts spanning low-to-high FAP expression and improved tumor selectivity index versus a synthetic Enhertu comparator.

Mechanistic Rationale

Strong. FAP-stromal-targeting and topoisomerase-I payload chemistry are both individually well-characterized. The translational track record of the broader FAP-PDC class remains unproven.

Research Gaps & Open Questions

What the current literature has not yet settled about AVA6103:

  • 01Human PK, safety, and tolerability — all to be defined in FOCUS-01.
  • 02Linker cleavage kinetics in human tumors — whether sufficient FAPα activity exists across the targeted tumor types to drive therapeutic exatecan release.
  • 03Comparative activity versus deruxtecan ADCs — the AACR 2026 comparator was synthetic, not a randomized head-to-head.
  • 04Optimal tumor-type selection — pancreatic, cervical, gastric, and SCLC are being explored in parallel, with response heterogeneity expected.
  • 05ILD signal monitoring — whether the topoisomerase-I payload carries the same ILD risk in a PDC format as it does in the deruxtecan ADC class.

Forms & Administration

Intravenous infusion in FOCUS-01. Investigational. Not commercially available. No compounded or research-chemical sources are legitimate.

Dosing & Protocols

The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.

Typical Range

FOCUS-01 dose-escalation pending. Both Q3W and Q2W schedules are being explored using BOIN methodology.

Frequency

IV infusion every 2 or 3 weeks depending on cohort.

Timing Considerations

No specific timing requirements: can be administered at any time of day, with or without food, and is not tied to exercise timing. Consistency matters more than the specific clock — dose at roughly the same time each day (or same day each week, for weekly protocols) to keep exposure steady.

Cycle Length

Standard oncology cycle structure per FOCUS-01 protocol.

Protocol Notes

AVA6103 is in early clinical development and is not commercially available. Eligible patients in FAP-expressing solid tumors may discuss FOCUS-01 enrollment with their oncologist.

AVA6103 is investigational and Phase 1 stage. Oncology indication; specialty oncology supervision required for any clinical trial participation.

Timeline of Effects

Onset

Standard cycle response assessment — initial response evaluation typically at 6–9 weeks (2–3 cycles).

Peak Effect

To be characterized in Phase 1 expansion and any future Phase 2 cohorts.

After Discontinuation

Pharmacological clearance per exatecan PK; long-term durability data not yet available.

Common Questions

Who AVA6103 Is NOT For

Contraindications
  • Oncology trial enrollment only — outside FOCUS-01, no legitimate access.
  • Pregnancy and breastfeeding — chemotherapy contraindication.
  • Severe baseline myelosuppression — exatecan-class payloads carry myelotoxicity risk.
  • Active or prior interstitial lung disease — class concern carried over from deruxtecan ADCs that share the topoisomerase-I payload family.
  • Known hypersensitivity to camptothecin-class drugs or peptide conjugates.

Drug & Supplement Interactions

No drug interaction profile is established. Exatecan-class payloads are partially metabolized by CYP3A4 and UGT enzymes (extrapolating from related camptothecin pharmacology), so co-administration of strong CYP3A4 modulators or UGT-affecting agents is a theoretical concern. FOCUS-01 protocol exclusions will define the practical interaction list as the program progresses.

Safety Profile

Safety Information

Common Side Effects

Phase 1 emergent — typical exatecan-related toxicities including myelosuppression, neutropenia, and GI effects would be anticipated at deprotected doses; specific tolerability profile pending readout

Cautions

  • Investigational — Phase 1 stage with no published human data yet
  • Oncology drug — managed under specialty oncology care only
  • Exatecan/topoisomerase-I payloads carry interstitial lung disease (ILD) signal seen across the deruxtecan ADC class — relevance to AVA6103 unknown

What We Don't Know

Human safety, tolerability, PK, and activity profile — all to be characterized in FOCUS-01 (NCT07454642).

Myths & Misconceptions

Myth

AVA6103 is Enhertu without the antibody.

Reality

AVA6103 shares the exatecan payload family with Enhertu's DXd, but the targeting strategy is fundamentally different. Enhertu targets HER2 on the tumor cell surface; AVA6103 targets FAP on stromal cancer-associated fibroblasts. The tumor populations that respond — and the resistance mechanisms — are not interchangeable.

Myth

Because AVA6103 uses a popular payload, it will work in many cancers.

Reality

Payload identity does not determine clinical success — delivery does. Whether AVA6103 reaches therapeutic exatecan concentrations in human tumors depends on FAPα expression density, tumor accessibility, and linker cleavage efficiency in human biology. The track record of FAP-activated drug delivery in clinical trials is still being written.

Myth

Avacta data showing AVA6103 beats Enhertu means it's already superior.

Reality

The AACR 2026 comparator was a synthetic Enhertu arm in preclinical xenografts — a useful internal benchmark, not a randomized human comparison. Preclinical superiority signals routinely fail to translate. Treat the preclinical data as platform validation, not clinical superiority.

Published Research

5 studies

Quick Facts

Class
FAP-Activated Peptide-Drug Conjugate
Tier
D
Evidence
Limited
Safety
Limited Data
Updated
May 2026
Citations
5PubMed

Also known as

FAP-ExdFAP-exatecanAvacta FAP-exatecan

Tags

InvestigationalOncologyPeptide-Drug ConjugateFAP-ActivatedTumor MicroenvironmentPhase 1Exatecan

Evidence Score

Overall Confidence25%

Clinical Trials

View Clinical Trials

Links to ClinicalTrials.gov for reference. Listing does not imply endorsement.