Micreos marks millions for endolysins

THE HAGUE, Netherlands—Dutch biotechnology company Micreos announced today that it has secured €30 million in funding to accelerate the development of its endolysin technology, reportedly set to replace antibiotics. Proceeds are earmarked for the clinical development program of its endolysin XZ.700 and the U.S. launch of its breakthrough OTC Gladskin product.

According to the World Health Organization, antibiotic resistance is one of the world’s biggest health threats. The call for true alternatives is more pressing than ever. Antibiotics do not distinguish between bad and good bacteria, and their use induces resistance.

According to the Micreos website, “Micreos’ proprietary technology is based partly on principles and mechanisms derived from nature, and used by the natural enemy of bacteria, phages. Phages kill roughly half of all bacteria on the planet every two days when they use bacteria as a host to reproduce.”

Phages and bacteria have co-evolved over millions of years, and as bacterial species have evolved over time, their respective phages have also. Enzymes called endolysins help open the bacterial cell wall from the inside in order to release new phages from their bacterial host cells, killing the bacterial cell in the process.

“As this step is essential for the reproduction cycle of phages, over time it has been perfected by targeting the essential parts of the bacterial cell wall - which do not mutate. This is why scientists do not expect emergence of resistance against endolysins,” the website continues.

Endolysins have three distinct features: the ability to target only unwanted bacteria while preserving the microbiome, which is essential for our health; the ability to kill antibiotic resistant strains of bacteria; and researchers do not expect the emergence of any resistance against endolysins. Endolysin technology opens a new therapeutic window for treatment of chronic inflammatory conditions, such as atopic dermatitis and persistent wound infections, including those caused by MRSA.

“The company’s proprietary endolysin XZ.700 is in clinical development for registration as a pharmaceutical product for various different indications. XZ.700 specifically kills S. aureus, now established as a major trigger for flares in eczema,” says the website. “Atopic Dermatitis is the first targeted XZ.700 indication. A combined Phase I/II trial is scheduled to start in 2020.”

Micreos’ Staphefekt SA.100 is the world’s first endolysin approved for human use. It selectively targets Staphylococcus aureus, which is a major trigger of eczema and other inflammatory skin conditions.

“Since its introduction, Gladskin has helped over 100,000 people in Europe with eczema, acne, and rosacea, many of them reporting a life-changing impact,” said Skyler Stein, head of Gladskin USA. “Gladskin is pioneering the use of endolysins to rebalance the skin microbiome and improve skin health.” Chosen as Europe’s Most Impactful Innovation 2018, Gladskin is now preparing its launch in the United States.

The €30 million funding includes a non-dilutive €5.4 million Innovation Credit granted by the Dutch Ministry of Economic Affairs. Micreos has conducted several studies with Gladskin, including trials on eczema, acne and rosacea. Studies in orphan indications with a high unmet need, like primary immune deficiencies and Netherton disease, are ongoing.

Micreos has production and R&D centers for endolysins in Bilthoven and for phages in Wageningen. Micreos maintains a long-term collaboration with ETH Zurich and Prof. Loessner in Switzerland and numerous medical and technology centers, including Erasmus MC in Rotterdam, the Public Health Lab Kennemerland, the Dutch Burn Centers in Beverwijk, Copenhagen University and many others.

“This funding from existing and new investors will advance the adoption of our endolysin technology and help us reach the millions who stand to benefit,” noted Micreos CEO Mark Offerhaus. “We are exploring partnerships to further accelerate the commercialization of our technology.”