These days, when we talk about emerging cancer therapies, we’re mostly talking about personalised or precision medicine. In contrast to the era of ‘one-size-fits-all’ treatments, today’s new crop of immunotherapy drugs are targeted at specific genetic changes. Two people with the same cancer might end up requiring very different drugs.
This fast-maturing field appears to hold great promise for cancer care. As more drugs hit the market, the benefits for patients are becoming apparent and survival rates are improving across multiple cancer types.
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By GlobalDataAs a result, the concept of a ‘universal cancer treatment’ may seem far-fetched. However, a drug that could benefit all cancer patients – killing the cancer without harming the patient – is perhaps still the holy grail of oncology research.
For Barcelona-based startup Peptomyc, it is more than a pipe dream. The company’s therapy, Oomomyc, has been successfully tested on mice and is on course to move into human trials next year.
“We have high hopes for Omomyc,” says Peptomyc CEO Professor Laura Soucek. “It could be applicable to multiple types of cancer, and we won’t need to separate patients depending on the mutation they carry because this is possibly going to be effective in all of them.”
She points out that, over the last decade or so, we’ve learnt that the best results in cancer treatment come about as a result of combining several different therapies. The problem is that combining drugs adds more toxicity.
“Our preliminary studies suggest that Omomyc doesn’t add any toxicity, which means it could be combined with lots of other cancer treatments that are out there,” she says. “In that sense it’s a revolutionary approach.”
An undruggable target?
The idea for Omomyc first arose in the 1990s, when Soucek was a student. She had been studying the Myc protein, which is central to the functioning of cancer cells, but was widely considered an ‘undruggable’ target.
“The protein doesn’t have a proper structure – it changes shape all the time,” she explains. “So if you think inhibiting Myc could be done with a simple small molecule that recognises it, that’s not going to happen. It’d be like designing a key for a lock that changes shape all the time. The key’s not going to work.”
On top of that, the Myc protein is buried deep in the cell nucleus, beyond the reach of most drugs. And since it is present in normal cells as well as tumour cells, scientists assumed that inhibiting the protein would result in catastrophic side effects.
“Myc acts as a music director inside the nucleus of the cell – it decides which genes should be turned on and off when a cell needs to divide,” says Soucek. “In normal physiological conditions, it is turned on only when a cell needs to divide, but it gets turned off when its job is done. So you can imagine this function becomes really advantageous for cancer cells, which hijack Myc so that it drives their operation all the time.”
Despite these obstacles, Soucek suspected that the orthodoxy surrounding Myc might be wrong. The reason, simply put, was a lack of evidence.
“I realised there were no data in the literature showing that it wouldn’t work,” she says. “Nobody had tried it for fear that could go wrong – it was a real dogma – but I thought that maybe someone should try it instead of making an assumption. I guess that’s the right attitude for a scientist.”
The path to Peptomyc
Over the next few years, Soucek worked to design a peptide-based inhibitor, which she called Omomyc. This was modeled into the shape of a different protein, known as Max.
“While Myc doesn’t have a good structure, at some point it forms pairs with a partner called Max, creating a nice regimental structure that allows it to recognise DNA and regulate the transcription of genes,” Soucek says. “That’s when it becomes nasty in the case of cancer – when it’s partnered with Max. Omomyc is essentially a fake Max. It pulls Myc into pairs that are not active anymore, and are no longer able to instruct the cells to proliferate.”
Despite successfully designing the inhibitor, it took many years – and a lot of pushback – before her research was able to advance beyond the lab. Working as a cancer researcher at the Universitat Autonoma de Barcelona, Soucek was repeatedly told that Omomyc would never be a cancer therapy.
Luckily, her persistence paid off. Her postdoc student Eve-Marie Beaulieu (now CSO of Peptomyc) demonstrated that Omomyc could penetrate cell nuclei, and could be delivered directly to tumour cells as a drug. Soucek and Beaulieu co-founded Peptomyc in 2014.
“We were able to found the company only after a long journey and a lot of obstacles,” she says. “After putting our savings in, we went looking for funding. Talking to venture capitalists was really difficult as we had to translate our scientific language into something that was appealing to investors. We had to learn a new language and a new frame of mind.”
Supported by EIT Health, Soucek and Beaulieu moved out their comfort zone to acquire the necessary business skills. By 2016, they had received €1m in seed funding, followed by a €4.2m series A round in 2017. The team has subsequently become highly adept not just at speaking to investors, but also at curing cancer in mice.
“What we showed in mouse studies is that Omomyc is beneficial in different types of cancer,” says Soucek. “It doesn’t matter what the mutation is – all the types of cancer we looked at need Myc inside the nucleus to execute their programmes.”
The next step will be a Phase I trial in humans, which could get underway as early as next January. Soucek is hoping to guide the product through Phase I and II, before licensing it to a pharma partner that can sponsor a Phase III trial and bring the drug through to market. Initially, it will be trialled in patients with metastatic breast cancer and non-small cell lung cancer, which have some of the lowest survival rates.
This stage, says Soucek, is the ‘moment of truth’, following over 20 years of preliminary research. If the team succeeds, it could be to the benefit of all cancer patients.
“We hope we can attack all types of cancer, and the beauty is normal tissues will not suffer,” Soucek says. “We really want to offer something much gentler and more respectful of normal tissues.”
