Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.03.11.711127

Tuning the Structural Properties of a Single-Domain Antibody Scaffold for Improved Fibroblast Activation Protein Targeting

Abstract

Fibroblast activation protein (FAP) is an attractive target for the development of cancer theranostics due to its selective expression on cancer-associated fibroblasts (CAFs). While a number of small-molecule FAP inhibitors (FAPIs) have been developed, few biologics have been investigated as FAP targeting vectors. Camelid-derived single-domain antibodies, or variable-heavy-heavy domains (VHHs), offer a compelling alternative, combining high affinity with versatile engineering options. In this study, we first identified a novel anti-FAP VHH, F7, from an affinity-matured camelid phage display library. To investigate how valency and molecular weight affected target engagement and in vivo properties, F7 was engineered into three formats: a monomer (F7), a tethered dimer (F7D), and an Fc-fusion protein (F7-Fc). All three were specific for FAP with the two bivalent constructs demonstrating picomolar affinity. Positron emission tomography imaging in FAP-positive xenograft models revealed distinct pharmacokinetic profiles across constructs with notable differences in tumor uptake and clearance. F7 had rapid uptake and clearance resulting in significantly higher tumor uptake than FAPI-46. Low molecular weight bivalent F7D demonstrated similar kinetics but was retained by the tumor resulting in a high tumor-to-blood ratio with secondary uptake limited to clearance organs. The largest construct, F7-Fc, resulted in the highest tumor uptake and allowed for longitudinal imaging. Absorbed dose calculations confirmed that tumors received significantly higher radiation doses compared to normal tissues. These findings demonstrate that tuning VHH scaffold size and valency can improve biodistribution and retention, establishing F7-based constructs as promising targeting vectors for FAP.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Ott, K., Gallant, J., Kwon, O., Adeniyi, A., Bednarz, B., Barrett, K., Rosenkrans, Z., Mixdorf, J., Engle, J., Aluicio Sarduy, E., Hernandez, R. T., LeBeau, A.. 2026-03-13. Tuning the Structural Properties of a Single-Domain Antibody Scaffold for Improved Fibroblast Activation Protein Targeting. https://doi.org/10.64898/2026.03.11.711127

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

m6A-Driven Intratumoral Cholesterol Biosynthesis Fuels Castration-Resistant Prostate Cancer Progression

Both nuclear pore complexes (NPCs) and RNA N6-methyladenosine (m6A) machinery are indispensable for proper cellular function. Although their collaborative roles in the nuclear export of messenger RNAs (mRNAs) have been reported, it remains ambiguous whether and how this collaboration may contribute to cancer progression. Here we identify a functional cooperation between NPCs and m6A signaling that promotes the development of castration-resistant prostate cancer (CRPC). We showed that nuclear export of m6A-modified mRNAs, mediated by the interaction between RNA methyltransferase METTL3 and the nucleoporin NUP93, is functionally coupled to cholesterol biosynthesis. Given that cholesterol-fueled intratumoral androgen production is one of the mechanisms driving CRPC, we demonstrated that overexpression of the wild-type METTL3 or NUP93, but neither the enzymatically dead METTL3 nor the mutant NUP93 that loses METTL3-interacting capability, elevates intracellular levels of androgens, activates AR signaling under castrate condition, and promotes androgen-independent growth of prostate cancer cells both in vitro and in vivo. Importantly, pharmacological inhibition of METTL3 or targeted demethylation on mRNAs encoding key cholesterol biosynthesis enzymes effectively suppressed CRPC malignancy. Together, these findings uncover a therapeutically targetable m6A-METTL3-NUP93 axis that links nuclear mRNA export and metabolic reprogramming to fuel CRPC progression, providing a conceptually new strategy for the treatment of this lethal disease.

cancer biology↗

ST6Gal2 promotes α2,6-sialylation and aggressive phenotypes in neuroblastoma cells

Neuroblastoma is the most common extracranial solid tumor of childhood. Its clinical behavior ranges from spontaneous regression to lethal, treatment-refractory disease. Aberrant 2,6-sialylation contributes to aggressive phenotypes in many cancers, but the role of ST6Gal2, a neural-enriched 2,6-sialyltransferase, in neuroblastoma is largely unexplored. Here, we examine the clinical and functional significance of ST6Gal2 in neuroblastoma. In two independent public cohorts (SEQC, n=498; Kocak, n=649), high ST6GAL2 expression was associated with significantly worse overall and event-free survival. In the SEQC cohort, ST6GAL2 expression was higher in high-risk and MYCN-amplified tumors, varied across International Neuroblastoma Staging System stages, and correlated positively with a mesenchymal transcriptional signature (Spearman {rho}=0.181). The mesenchymal correlation was reproduced in the Kocak cohort ({rho}=0.204). Stable shRNA-mediated knockdown of ST6GAL2 in SK-N-AS and SK-N-BE(2) cells reduced proliferation and viability, impaired wound closure, and decreased migration and invasion. In preliminary experiments in SK-N-AS cells, ST6GAL2 knockdown reduced binding of Sambucus nigra agglutinin, consistent with a role for ST6Gal2 in 2,6-sialylation. Together, these findings link ST6Gal2 expression to aggressive clinical and transcriptional features and pro-tumorigenic phenotypes in neuroblastoma and nominate ST6Gal2-mediated sialylation as a candidate pathway for mechanistic study.

cancer biology↗

Unsupervised transcriptomic analysis of paired pre- and post-treatment specimens reveals divergent chemoimmunomodulatory induction trajectories in breast cancer

The immunomodulatory effects of chemotherapy (chemoimmunomodulation; CIM) are clinically consequential and heterogeneous, yet no systematic framework exists for classifying the immunomodulatory trajectory a tumor follows in response to treatment (CIM trajectory). Here, we present the CIM Induction Classifier (CIMIC), an unsupervised clustering pipeline leveraging delta gene expression across 3,189 CIM-related genes to classify specimens chemoimmunomodulatory trajectory. Applied to two pre- and post-chemotherapy breast cancer (BC) datasets (NKI/SMC, N = 36; NEO, N = 19) and nine epirubicin-perturbed triple-negative BC (TNBC) cell lines, CIMIC identified two divergent CIM trajectories: a functional CIM (Fun-CIM) trajectory, broadly conserved across tumors and cell lines and characterized by induction of inflammatory cell death, antigen presentation, viral mimicry, and adaptive immune activation programs, and a dysfunctional CIM (Dys-CIM) trajectory, characterized by induction of proteostatic and metabolic stress-adaptation programs, reduced immune cell abundances and cytotoxic activity, and enrichment of aggressive BC subtypes. Using survival and longitudinal transcriptomic data in NKI/SMC (N = 20), treatment-induced increases in Fun-CIM-associated genes and ssGSEA scores were associated with reduced recurrence, whereas Dys-CIM-associated genes and scores were associated with increased recurrence. In multivariable analyses within independent chemotherapy-treated BC cohorts (METABRIC, N = 412; SCAN-B, N = 2,462), higher baseline Fun-CIM ssGSEA scores were associated with better outcomes, whereas higher baseline Dys-CIM ssGSEA scores were associated with worse outcomes. These findings establish CIM as a dynamic, trajectory-level process and position CIMIC as a framework for defining CIM trajectories and supporting future efforts to identify predictors, mechanisms, and therapeutic strategies that maximize beneficial CIM.

cancer biology↗