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Profacgen's Targeted Protein Degradation Services deliver comprehensive, integrated solutions spanning degrader discovery, E3 ligase development, ubiquitination analysis, and in vitro/in vivo evaluation, enabling accelerated advancement of PROTACs, molecular glues, and emerging degradation modalities from concept to clinic.
As one of the well-known service providers in the biotechnology field, Profacgen keeps in step with cutting-edge biological research and quickly responds to customer demands for new methods and techniques. We provide personalized targeted protein degradation services against proteins of interest (POIs), offering a promising therapeutic strategy for drug discovery through redirecting cellular protein homeostasis machinery. Our experienced team, based on many years of research in biochemistry and structural biology, is confident in delivering optimal solutions to help you succeed.
What Is Targeted Protein Degradation?
Targeted protein degradation is an emerging therapeutic strategy that eliminates disease-causing proteins by co-opting the cell's natural protein disposal machinery. Unlike traditional inhibitors that merely block protein function, degraders induce complete protein removal, offering superior efficacy and the ability to target previously undruggable proteins:
Ubiquitin-Proteasome System (UPS): The primary degradation pathway for intracellular proteins. E3 ubiquitin ligases tag substrate proteins with ubiquitin chains, directing them to the 26S proteasome for unfolding and proteolysis. PROTACs and molecular glues hijack this system to eliminate POIs
Lysosomal Degradation: An alternative pathway for extracellular and membrane-associated proteins. LYTACs (lysosome-targeting chimeras) and AUTACs (autophagy-targeting chimeras) redirect POIs to the lysosome for degradation, expanding the targetable protein space
Selective Target Elimination: The hallmark of targeted protein degradation. By recruiting specific E3 ligases or lysosomal receptors, degraders achieve exquisite selectivity for POIs while sparing closely related proteins, minimizing off-target toxicity and maximizing therapeutic windows
Figure 1. Summary of the ubiquitin system and targeted protein degradation mechanisms. (Tsai et al., 2024)
Our Service Portfolio
Profacgen offers a comprehensive suite of targeted protein degradation services, organized into five integrated modules:
End-to-end degrader discovery from target assessment and ligand identification through degrader design, synthesis, and cellular validation. Services include small molecule ligand screening, peptide design for E3 ligase or target protein, custom peptide and compound synthesis, novel E3 ligase discovery, and ligand discovery and design.
Comprehensive protein production and characterization supporting degrader discovery. Services include E3 ligase or target protein expression and purification, E3 ligase activity assays, and custom protein ubiquitination services with rigorous quality control.
Quantitative analysis of ubiquitin-mediated protein modification and degradation. Services include in vitro and cell-based ubiquitination assays, ubiquitination site mapping by mass spectrometry, polyubiquitin chain analysis, and real-time degradation kinetics measurement.
Integrated in vitro and in vivo assessment of degrader performance. Services include binding affinity measurement, ternary complex formation analysis, protein degradation assays, ubiquitination assays, permeability assessment, and in vivo pharmacokinetic and efficacy studies.
Specialized technologies and reagents enabling diverse degradation modalities. Services include HaloPROTAC, LYTAC, AUTAC, ATTEC, hydrophobic tag, and destabilization domain platforms for customized degradation applications.
Targeted Protein Degradation Workflow
Profacgen implements a systematic, stage-gated workflow that progresses from target identification through lead optimization:
Targeted Protein Degradation Technologies
Profacgen supports diverse degradation modalities beyond traditional PROTACs, enabling tailored strategies for distinct target classes and cellular contexts:
Technology
Description
PROTAC
Heterobifunctional small molecules recruiting E3 ubiquitin ligases to intracellular targets for proteasomal degradation. The most established modality with broad target scope and clinical validation.
Molecular Glues
Monovalent small molecules that induce novel protein-protein interactions between target and E3 ligase, enabling degradation without bipartite design. Superior drug-like properties but more challenging discovery.
A tag-based system utilizing HaloTag fusion proteins and chloroalkane-linked ligands for conditional, reversible target degradation. Enables rapid target validation and temporal control of degradation.
Lysosome-targeting chimeras that recruit extracellular and membrane-associated proteins to the mannose-6-phosphate receptor for lysosomal degradation. Expands degradable target space beyond the proteasome.
Autophagy-targeting chimeras that tag targets with K63-linked ubiquitin chains for selective autophagy. Enables degradation of organelles, protein aggregates, and pathogens.
Autophagosome-tethering compounds that directly bridge targets to LC3 on autophagosome membranes, bypassing ubiquitination. Suitable for degrading non-protein cargoes including lipids and organelles.
Fusion of hydrophobic moieties to target proteins, mimicking misfolded protein states and triggering chaperone-mediated degradation. Enables degradation of proteins lacking ligandable surfaces.
Genetically encoded fusion tags that conditionally stabilize or destabilize target proteins upon small molecule administration. Provides precise temporal and reversible control for mechanistic studies.
Applications
Targeted protein degradation enables transformative therapeutic strategies across major disease areas:
Oncology: Degradation of oncogenic drivers, transcription factors, and epigenetic regulators; overcoming resistance to kinase inhibitors; targeting tumor suppressor loss-of-function mechanisms; and selective elimination of cancer-specific protein isoforms
Neurodegenerative diseases: Removal of aggregated proteins (tau, α-synuclein, huntingtin); modulation of protein quality control pathways; and targeting neuroinflammation mediators. Brain-penetrant degraders offer disease-modifying potential for Alzheimer's, Parkinson's, and Huntington's diseases
Inflammation: Targeted elimination of inflammatory mediators, immune checkpoint regulators, and signaling scaffold proteins. Degradation offers prolonged pharmacodynamic effects compared to inhibition, reducing dosing frequency and improving compliance
Undruggable targets: Functional modulation of proteins lacking enzymatic active sites or druggable pockets, including transcription factors, non-kinase scaffolds, protein-protein interaction hubs, and RNA-binding proteins previously considered inaccessible to small-molecule intervention
Why Choose Profacgen for Targeted Protein Degradation?
Comprehensive Integrated Platform: Five specialized service modules spanning discovery, development, ubiquitination, evaluation, and platform technologies within a single provider, eliminating handoff inefficiencies and accelerating program timelines.
Cutting-Edge Modality Support: Beyond traditional PROTACs, we support molecular glues, LYTACs, AUTACs, ATTECs, hydrophobic tags, and destabilization domains, enabling tailored strategies for any target class.
Deep Scientific Expertise: Our team combines decades of experience in biochemistry, structural biology, E3 ligase biology, and medicinal chemistry with proven track records in degrader discovery and optimization.
Responsive and Collaborative: We work closely with clients from project inception through data delivery, with 24/5 expert support, transparent communication, and flexible engagement models.
Frequently Asked Questions (FAQs)
Q: What is the difference between PROTACs and molecular glues?
A: PROTACs are heterobifunctional molecules with two ligands connected by a linker, recruiting E3 ligase to target. Molecular glues are monovalent small molecules inducing novel protein-protein interactions between target and E3. PROTACs offer modular design; glues offer superior drug-like properties but require serendipitous discovery.
Q: Can degraders target proteins without druggable pockets?
A: Yes. Degraders can eliminate transcription factors, scaffold proteins, and PPI hubs lacking enzymatic active sites. LYTACs and AUTACs further expand scope to extracellular and membrane proteins. Hydrophobic tags and destabilization domains enable degradation of virtually any protein.
Q: Which degradation modality should I choose for my target?
A: Intracellular targets are typically addressed by PROTACs or molecular glues. Extracellular and membrane targets require LYTACs. Protein aggregates and organelles suit AUTACs or ATTECs. Conditional or reversible degradation employs HaloPROTACs or destabilization domains. We guide modality selection based on target biology.
Q: How long does a typical degrader discovery program take?
A: From target validation to lead candidate, PROTAC programs typically require 12–18 months. Molecular glue discovery is more variable (18–24 months). LYTAC and specialized modalities may require additional platform development. Our integrated services and established platforms accelerate timelines compared to fragmented outsourcing.
Q: What is the difference between UPS and lysosomal degradation?
A: The ubiquitin-proteasome system (UPS) degrades intracellular proteins tagged with K48-linked ubiquitin chains. The lysosome degrades extracellular proteins, membrane proteins, and organelles via autophagy or receptor-mediated routing. PROTACs and glues use UPS; LYTACs and AUTACs use lysosomal pathways.
Q: Can I start with a single service module or must I use the full platform?
A: Our services are modular and flexible. You can engage any single service or combination based on your program needs. Many clients begin with discovery or evaluation services and expand to integrated campaigns as programs mature. We provide seamless transitions between modules.
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Figure 1. Summary of the ubiquitin system and targeted protein degradation mechanisms. (Tsai et al., 2024)
