Self-Destruct Sequence

Co-Creation – SRTD biotech GmbH

Cancer Medication can save lives, but they often damage healthy tissue along the way. For years, Bernd Hoffmann assumed that trade-off was unavoidable. Then he began sketching a molecule that could tell healthy cells from diseased ones.

June 2026

The problem with cancer medications

The problem with cancer drugs is not that they fail. Often, it is precisely that they work. They attack cells that divide quickly - the hallmark of a tumour, but also a feature of hair follicles, skin and mucous membranes. Some treatments can also damage healthy cells in the liver, heart and gastrointestinal tract. For physicians, these side effects can be the price of saving a life. For decades, medicine has tried to lower that price: to hit cancer harder while harming less of the body around it. Only rarely has that promise fully held.

A Blank Sheet of Paper

Dr Bernd Hoffmann leads a research group at the Institute of Biological Information Processing - Mechanobiology. He has spent years studying how cells process information and how molecular mechanisms decide what happens inside them. In 2013, he and colleagues founded a company that sells transfection reagents - tools that help deliver molecules into cells. One day, a customer asked whether Hoffmann could develop a molecule that would enter every cell, but become active only in selected ones. "That is impossible," Hoffmann replied.

The customer asked him to think about it anyway. So he did. For a week, Hoffmann withdrew from the usual flow of work, stared at a blank sheet of paper and turned the problem over in his mind. Then something clicked. What took shape on the page was a molecular switch: a specially designed molecule built from several components. It would enter cells in an inactive state. Only if it recognised a diseased cell would it switch on. The technical term is selectively expressed RNA, or seRNA.

„Using the cell’s own RNA as a switch is completely new.“

— Dr. Bernd Hoffmann

A Molecular Lego Set

Since the COVID-19 pandemic, messenger RNA has become part of everyday language. In simple terms, mRNA is a set of instructions delivered into a cell, telling it to make a particular protein. But conventional mRNA is blunt: once a cell takes it up, the message is read.

Hoffmann’s seRNA works differently. The idea is almost disarmingly simple, and scientifically elegant: a modular molecular system assembled like Lego bricks. One brick acts as a sensor. It searches the inside of the cell for a genetic fingerprint - an RNA sequence found only in cancer cells. In a healthy cell, nothing happens. The seRNA stays silent and is broken down without leaving a trace.

If the sensor finds its target - in a cell from an aggressive glioblastoma, for example - the system snaps into action. The cell receives the command to produce a protein that kills it from within. The cancer cell is made to trigger its own destruction. "Using the cell’s own RNA as a switch is completely new," Hoffmann says.

The system has another crucial advantage: its building blocks can be exchanged. In principle, researchers can replace the sensor and retune the platform for another cancer type. Hoffmann believes his training helped him reach this point. He describes himself as an old-school molecular biologist. "When I trained, there were no preconfigured kits of substances for every possible application, as there often are today.

We first had to understand exactly how something worked before we could decide which components might fit together," he says. That habit of thinking from first principles became the basis for the sketch that led to seRNA.

„Nothing is more frustrating than having to tell people that we are not there yet.“

— Dr. Bernd Hoffmann

A Long, Expensive Road

In the lab, the principle worked in the very first experiment. "Success on the first attempt is extraordinary," Hoffmann says, still sounding surprised. He went on to found a new start-up, SRTD biotech. In mouse studies, the approach succeeded in making cells from glioblastoma - one of the deadliest forms of brain cancer - destroy themselves.

But the distance between a brilliant sketch and a therapy for patients is measured in years, regulatory hurdles and money. A single test series can cost around EUR 8 million. "You burn through millions without earning a single cent," Hoffmann says. It is a bet on the future - and an emotional one. Since early successes became known, desperate relatives of cancer patients have contacted him again and again. "Nothing is more frustrating than having to tell them that we are not there yet," he says.

That is why one aim matters especially to him: the therapy should, if it succeeds, remain affordable for public healthcare systems and available to patients broadly. While some modern cell therapies cost up to EUR 1 million per treatment, Hoffmann believes this treatment could eventually be offered for around EUR 6,000 per course.

Toward a Universal Therapy

The sketches have long since become patents. Hoffmann has also learned from his first company that scientific perfection and commercial timetables belong to different worlds. So he is making a move that many founders find difficult: he is stepping down as CEO of his own company. "You cannot do everything as well as people who have trained for it," he says. He is making room for an experienced pharmaceutical executive from the United States - someone used to navigating billion-euro deals.

As Chief Scientific Officer, Hoffmann is returning to the place where he believes he can push the technology forward fastest: the lab bench. There, he is working to move the system beyond brain tumours. Because the platform’s building blocks can be exchanged, he hopes one day to adapt it for liver cancer, hepatitis B and autoimmune diseases.

That will require patience. "Nine out of ten experiments usually come to nothing. You need an enormous tolerance for frustration. In the end, the person who can endure the most will be the most successful," Hoffmann says. Today, he is developing something he once believed was impossible.

Visit the SRTD Biotech website
The Self-Destruction of Glioblastoma – Press Release, January 8, 2025

The seRNA enters every cell—whether healthy or altered. The genetic blueprint it carries is locked and remains inactive.”

Because the sensor cannot find a matching counterpart in a healthy cell, the instruction remains inaccessible and the seRNA stays inactive. The cell then degrades it completely without leaving any residue within a short time.

In the cancer cell, the sensor finds its counterpart (purple) — the matching key to the instruction. Both bind to each other, triggering a reaction: the cell begins to partially degrade the seRNA — a mechanism that activates the molecular switch.

The exposed effector (orange) becomes active and releases the blueprint for a specific enzyme that the cancer cell produces itself. This enzyme initiates programmed cell death.

Green: Inside the cell, the sensor module scans the environment for a specific cancer marker. Only when it finds this exact counterpart (purple), it locks in and forms a double strand — the molecular signal: “target found".

Green and purple: This double-stranded structure acts as an alarm signal. It triggers the cell to partially degrade the seRNA. This is the key mechanism: only then is the safety lock removed and the molecular process initiated.

Orange: The effector releases the genetic blueprint for an enzyme that the cancer cell then produces itself — initiating its own programmed cell death. The key feature: the components are modular and can be adapted to different diseases.

In healthy cells, the matching key is absent. The blueprint remains locked, and the seRNA stays completely inactive. Without causing side effects, the molecule is naturally cleared from the body within hours, leaving no residues.

^{Image Credits: Forschungszentrum Jülich}

Mehrere Geräte, ein Gehirn und zerknülltes Papier auf orangefarbenem Hintergrund. (Mistral: Mistral Medium 3.5, 2026-06-30)

Perspectives: The new Issue

Some diagnoses change the way we view our own lives, often leading to a long road, full of uncertainty and unanswered questions.

In this issue, we meet researchers who are developing new approaches to treating cancer, chronic pain and other diseases. Their work is producing insights that could one day change how we view these diagnoses.

» Download Issue (German, PDF)