There is a protein on the surface of your red blood cells that malaria parasites have depended on for millions of years. They knock, and the door opens. Once inside, they multiply until the cell bursts, and the cycle begins again.

Ibex Biosciences found a way to lock the door.

The antibody they developed, called IBX13, binds to that protein—CD147—and simply sits there. (Reassuringly, this same target has been safely blocked by other antibodies in unrelated human trials.) The parasite arrives, finds the entrance blocked, and dies outside. No complicated biochemistry. No poison. Just a small, heat‑stable antibody from an alpaca, doing what antibodies do best: getting in the way.

What makes this worth paying attention to is not just that it works in mice. It works in human blood in Petri dishes. And it works in mice with human red blood cells circulating through their veins, a model that closely mirrors human infection. A single intravenous dose cleared the parasite completely. And it works at doses that leave the animals healthy and active, even at 50 times what would be needed for treatment.

Two Problems, One Antibody

The cancer program is different. For colon cancer, the antibody is not enough on its own. Cancer cells do not need CD147 to survive the way parasites do. The protein helps them grow and proliferate but blocking it does not kill them. You have to attach something that will.

Ibex attached monomethylauristatin F (MMAF), a toxin that stops cells from dividing. In animal studies, the resulting antibody-drug conjugate (ADC) produced potent antitumor activity after a single intravenous dose.

Ibex’s antibody binds tightly and stays bound, but once it binds to tumor cells, it is internalized via endocytosis and delivers its toxic payload. In the HT29 colorectal cancer model—a human tumor line grown in mice that resists standard of care chemotherapy—the antibody conjugate achieved 100% tumor elimination with a single 10 mg/kg dose by Day 22 (ED₅₀ = 0.52 mg/kg). The animals showed no signs of distress in this study.

The same antibody, carrying the same toxin (IBX13-ADC), also worked against melanoma and ovarian cancer cells in other animal studies. The platform is broader than one indication and could be applied to cancers that overexpress the CD147 protein.

The Camelid Advantage

Most therapeutic antibodies are shaped like a Y, with two heavy chains and two light chains. Camels and alpacas produce a simpler version: two heavy chains, no light chains. The part that binds to targets is correspondingly smaller and more stable.

The smaller size lets it reach epitopes that conventional antibodies may not. It also makes the molecule more resistant to heat. Traditional antibodies require refrigeration from the manufacturing plant to the patient’s arm—the cold chain. In Africa, where malaria kills more than 450,000 children every year, the cold chain is expensive and unreliable. A heat‑stable antibody can be shipped and stored without it. That stability determines whether a therapy reaches village clinics and hospitals in a functional state.

On the IP front, Ibex secures its anti‑CD147 antibodies with composition‑of‑matter claims defined by exact CDR sequences (the short protein loops that determine what an antibody binds to), delivering durable, molecule‑level protection at a time when courts are weakening broad, function‑based antibody patents. This gives Ibex defensible IP with clear freedom to operate and strong barriers to entry.

The Founders

Murat Croci and Michael Karlin spent years consulting for early‑stage biotech companies, watching scientists make discoveries but fail to commercialize them because they couldn’t navigate the business side. They began to ask what would happen if they started with the business model and brought in the science later. They read widely across disciplines, looking for findings fully proven in one field, but completely overlooked in another. Then came a discovery about a receptor in cancer biology might have implications for infectious disease that the original researchers never considered.

After several years, Croci and Karlin realized they needed someone who understood the lab work well enough to test their ideas. They found Vidal de la Cruz, who spent decades in biotechnology drug development across all levels of early‑stages and was a co‑inventor of the phage display technology that underpinned the 2018 Nobel Prize in Chemistry. Vidal joined as chief scientific officer and as a co‑founder.

The Malaria Data

The Art of Discovery, a contract research organization in Spain, ran the decisive animal study. They used mice engrafted with human red blood cells—a model that more faithfully replicates human infection than standard mouse malaria. A single intravenous dose of just 150 micrograms (0.00015 grams) of IBX13 per mouse cleared the parasite completely.

Studies confirmed that IBX13 binds CD147 on the surface of red blood cells and stays bound. The parasite cannot dislodge it or evolve around it because the target is not on the parasite. The parasite evolves; the human receptor does not. Resistance would require the parasite to find a new route into the cell, which would require a fundamental change in its biology.

Heat stability was confirmed separately. IBX13 remained active after weeks at temperatures that would destroy conventional antibodies. In malaria‑endemic regions, where supply chains are long and electricity is unreliable, this shifts the calculus of what treatment is possible.

The Cancer Data

Melior Discovery, a U.S. contract research organization, ran a chemo‑resistant HT29 human colorectal cancer xenograft study in athymic nude mice to evaluate the cleavable IBX13–MMAF ADC. They administered single intravenous doses ranging from 0.1 to 10 mg/kg once tumors reached ~100–150 mm³. A single 10 mg/kg dose achieved 100% tumor elimination by Day 22 (ED₅₀ = 0.52 mg/kg) with no significant weight loss.

What Comes Next

Ibex is raising up to $20 million to move both programs into human trials. The money will cover manufacturing, toxicology studies required by the FDA, and the first phase of clinical testing. Phase 1b trials are designed primarily for safety and efficacy. If IBX13 and IBX13‑ADC behave in humans as they have in animal studies, they will show few adverse effects (if any) and definitive outcomes against malaria and colorectal cancer.

Success in Phase 1 would position the company for partnership or further financing to move into further clinical studies. The malaria program, because it uses the naked antibody without toxin, would move faster. The cancer program, while more complex, addresses a much larger market. Colorectal cancer kills 900,000 people worldwide each year. The five‑year survival rate for Stage IV disease in the United States is 12.5%.

A Strategic Shift

Ibex’s malaria strategy focuses on access as the path to eradication. By blocking the receptor the parasite depends on, the therapy prevents invasion at the outset or clears an existing invasion; if the parasite can’t enter another red blood cell within about one minute, the infection ends.

In cancer, the strategy relies on the antibody’s ability to be endocytosed by tumor cells that overexpress the target. Once internalized, the toxin is released, killing the cells and, ultimately, the tumor.

Both approaches rest on the same insight: find what the disease needs and take it away. The parasite needs a door. The cancer needs a receptor that helps it grow. Exploit that dependence, and the disease falters.

Learn more about Ibex Biosciences here: https://www.ibex.bio/