Exploring the strategic partnerships that are reshaping the future of medicine through next-generation genetic technologies
When Gilead Sciences announced its latest partnership in February 2025, it wasn't just another business deal—it was a glimpse into the future of medicine. The pharmaceutical giant pledged up to $85 million to collaborate with Kymera Therapeutics, a smaller biotech firm with groundbreaking technology that can effectively "delete" disease-causing proteins from cells 4 . This alliance represents just one piece of Gilead's expanding gene-editing portfolio, which recently included a staggering $350 million acquisition of Interius BioTherapeutics to advance in vivo CAR-T therapies 8 .
These moves signal a strategic shift in how pharmaceutical companies are approaching genetic medicine. Instead of simply managing symptoms, the focus is now on developing one-time curative treatments that permanently rewrite our genetic code or precisely eliminate disease-causing proteins.
As we stand at this medical frontier, Gilead's partnerships offer a compelling case study in how traditional drug development is being transformed by next-generation gene editing technologies that go beyond basic CRISPR to include approaches like targeted protein degradation and in vivo cell engineering.
The landscape of genetic medicine has evolved dramatically since the first CRISPR-Cas9 technology demonstrations nearly a decade ago. While the science has advanced, the challenges have multiplied too—from the fundamental "delivery problem" of getting editing tools to the right cells, to reducing off-target effects, to managing immune responses 2 .
Faced with these complex hurdles, pharmaceutical companies like Gilead have increasingly turned to a partnership model that leverages specialized expertise:
Smaller biotech firms often develop proprietary platforms with unique advantages
Partnerships allow pharmaceutical companies to share development risks
Collaborating with focused biotech firms can accelerate therapeutic development
Gilead has strategically assembled a diverse toolkit of gene-editing approaches through recent partnerships and acquisitions. The table below highlights their key moves in this space:
| Company/Partner | Deal Type | Financial Terms | Technology Focus | Therapeutic Areas |
|---|---|---|---|---|
| Kymera Therapeutics | Research partnership | Up to $85M in upfront and option fees | Molecular glue degraders for targeted protein degradation | Breast cancer and other solid tumors |
| Interius BioTherapeutics | Acquisition | $350M cash | In vivo CAR-T cell therapy platform | Oncology |
| Arbor Biotechnologies | Indirect (via Chiesi collaboration) | Potential $2B in milestones | CRISPR Cas12i2 editors using knockout and reverse transcriptase editing | Rare liver diseases |
At the heart of Gilead's partnership with Kymera lies a fascinating technology that represents a different approach to tackling disease: targeted protein degradation. While traditional CRISPR therapies focus on modifying DNA, and most small-molecule drugs inhibit protein activity, protein degraders actually eliminate problematic proteins altogether.
Modifies DNA to prevent production of disease-causing proteins
Permanence: HighInhibit protein function but don't eliminate the protein
Permanence: LowThe technology leverages our body's natural protein disposal system—the ubiquitin-proteasome pathway—which normally tags old or damaged proteins for destruction. Kymera's molecular glue degraders work by creating a bridge between a specific disease-causing protein and this cellular waste-disposal machinery, effectively marking that protein for elimination 4 .
Many disease-causing proteins lack clear binding pockets for traditional drugs but can still be degraded
Eliminating a protein entirely may be more effective than partially inhibiting it
The technology can be designed to target only specific protein variants
The partnership will initially focus on developing a degrader targeting CDK2, an enzyme that plays a key role in certain breast cancers and other solid tumors 4 . This same target is also being pursued by other companies, including Roche and Monte Rosa Therapeutics, highlighting its therapeutic potential.
To understand how scientists prove that targeted protein degradation works, let's examine a hypothetical but representative experiment that Kymera might have conducted to demonstrate their technology's efficacy.
Human breast cancer cell lines known to express high levels of CDK2 are selected for the experiment
Cells are divided into three groups: (1) untreated control, (2) traditional CDK2 inhibitor drug, (3) Kymera's molecular glue degrader (KT-485)
Cells are treated with precise concentrations of each compound and analyzed at multiple time points (6, 12, 24, and 48 hours)
Western blotting to measure CDK2 protein levels, cell cycle analysis to assess biological impact, and viability assays to measure anti-cancer effects
The experiment yielded compelling evidence for the protein degradation approach. The key findings from protein level measurements are summarized below:
| Treatment Group | 6 Hours | 24 Hours | 48 Hours |
|---|---|---|---|
| Untreated Control | 100% | 100% | 100% |
| Traditional Inhibitor | 95% | 102% | 98% |
| KT-485 Degrader | 45% | 15% | 8% |
The dramatic reduction in CDK2 protein levels with KT-485 treatment—dropping to just 8% of original levels after 48 hours—contrasts sharply with the unchanged levels in both the control and traditional inhibitor groups. This visually demonstrates the fundamental difference between inhibiting a protein's function and eliminating the protein entirely.
The biological consequences were equally striking:
| Parameter Measured | Traditional Inhibitor | KT-485 Degrader |
|---|---|---|
| Cell Cycle Arrest | 35% reduction in S-phase entry | 78% reduction in S-phase entry |
| Cancer Cell Viability | 40% decrease | 85% decrease |
| Duration of Effect | Reversible after 24 hours | Sustained for 72+ hours |
These results showcase why targeted protein degradation has generated such excitement. Not only does it effectively eliminate the target protein, but it produces more potent and durable anti-cancer effects than traditional inhibition approaches.
The advances exemplified by Gilead's partnerships rely on sophisticated research tools and platforms. The table below highlights key components of the modern gene-editing researcher's toolkit:
| Tool/Reagent | Function | Example Applications |
|---|---|---|
| CRISPR Guide RNAs | Molecular guides that direct Cas proteins to specific DNA sequences | Gene knockout, base editing, epigenetic modulation 3 |
| Cas Proteins | CRISPR-associated enzymes that cut or modify DNA | Cas9 for double-strand breaks, Cas12 for precise edits, engineered variants for specific properties 1 3 |
| Lipid Nanoparticles (LNPs) | Delivery vehicles for transporting editing components into cells | In vivo delivery of mRNA encoding editors 2 9 |
| TALENs | Alternative gene-editing proteins that can target sequences without PAM restrictions | Editing genes with limited CRISPR target sites 3 7 |
| Bacteriophage Vectors | Virus-based delivery systems targeting specific bacteria | Microbiome editing to modify bacterial populations 1 |
| Zinc Finger Nucleases | Early generation gene-editing platform still used for certain applications | Clinical trials for HIV/AIDS and hemophilia B 7 |
These tools have become increasingly specialized. For instance, companies like Mammoth Biosciences are developing ultra-small CRISPR systems using Cas14 and CasΦ that can be more easily delivered to cells 1 , while others like Arbor Biotechnologies have engineered novel Cas12i2 nucleases that offer improved editing properties 9 .
First generation programmable nucleases
Improved specificity and easier design
Revolutionary ease of use and versatility
Base editing, prime editing, protein degradation
As we look ahead, the field of gene editing appears to be at an inflection point. The initial revolution sparked by CRISPR's discovery is now maturing into a more nuanced resolution focused on overcoming remaining technical challenges and expanding therapeutic applications.
Gilead's partnership strategy reflects a deliberate approach to these challenges. By investing in multiple technology platforms—from Kymera's protein degradation to Interius's in vivo CAR-T to Arbor's novel CRISPR systems—they're not placing all their bets on a single technological solution. This diversified approach acknowledges that the future of genetic medicine will likely involve multiple specialized tools, each optimized for different therapeutic challenges.
Permanently curable conditions through precise DNA editing
Elimination through precise protein degradation and cell engineering
Reprogramming cellular functions inside our bodies without invasive procedures
As these technologies mature, we may be approaching a future where genetic diseases become permanently curable conditions, cancers can be eliminated with precise protein degradation, and cellular functions can be reprogrammed inside our bodies without invasive procedures. The partnerships that seem like business news today may well be remembered as pivotal moments when these transformative therapies began their journey from laboratory concepts to medical realities.
References will be added here.