CHICAGO — Decades of research have failed to uncover a therapeutic answer to one of the most well-known genetic drivers of cancer. Yet Amgen thinks it’s broken through with an early-stage drug that, in initial results presented Monday at the American Society of Clinical Oncology’s annual meeting, spurred tumors to shrink in five of 10 lung cancer patients.

The therapy’s target is KRAS, an oncogene known to be behind many lung, pancreatic and colorectal cancers. Past efforts to develop an effective treatment have consistently come up short — a history that makes Amgen’s data noteworthy despite coming from just a handful of patients.

“Nothing’s worked,” said Roy Herbst, chief of medical oncology at the Yale Cancer Center, in an interview. “KRAS is like the master of a symphony. It turns on so many different pathways.” Herbst consults with many drugmakers, but not Amgen.

Amgen’s drug, called AMG 510, is the first of its kind to reach clinical testing. It works by binding to what the company describes as a “hidden groove” on the protein produced by the mutated KRAS gene. With AMG 510 locked on, the protein is inactivated, in theory shutting down the signals it sends to trigger cell division and tumor growth.

AMG 510 is aimed at a specific type of KRAS mutation called G12C, which occurs in roughly 13% of non-small cell lung cancers, 3% to 5% of colorectal cancers, and between 1% and 3% of other solid tumors.

That prevalence, coupled with KRAS’ reputation as “undruggable,” makes AMG 510 particularly crucial for Amgen. Expectations on Wall Street are already high, even though clinical testing began less than a year ago.

“We’ve been able to execute this study extremely quickly,” said Dirk Nagorsen, head of early oncology development at Amgen, in an interview. “Now here we are at ASCO presenting clinical data.”

So far, 35 patients have enrolled in Amgen’s Phase 1 study across 4 doses of AMG 510. All but two of those participants had heavily pretreated lung or colorectal cancer, and the presence of the KRAS G12C mutation was confirmed by gene sequencing.

No dose-limiting toxicities were observed and no serious treatment-related adverse events occurred.

Among the 10 lung cancer patients evaluable for efficacy, five experienced partial responses to therapy, while four had stable disease. All patients who responded remain on therapy with follow-up stretching from seven weeks to more than six months.

One of the patients who saw a partial response by time of data cut-off later improved to a complete response, Amgen said.

“The fact that we’re seeing activity at this level is extraordinary,” said Yale’s Herbst, although he cautioned much is unknown.

“It’s still way too early. We don’t know the progression-free survival, we don’t know the duration of response,” he added.

Current treatment options for KRAS-driven lung cancer are platinum chemotherapy, immunotherapy and docetaxel, all of which spur responses in less than a fifth of patients.

“Anything with a response rate greater than 20% I would consider to be a major advance in the field,” said John Heymach, an oncologist at The University of Texas MD Anderson Cancer Center, in an interview. Heymach has consulted with more than a dozen drugmakers, but not Amgen.

But he added that he would want to see efficacy data from between 30 to 50 patients before feeling confident in the rate of response.

Results didn’t appear as positive in colorectal cancer, however, where 13 of 18 evaluable patients had stable disease. Amgen didn’t report any tumor responses.

Still, Amgen’s data comes in ahead of what Wall Street analysts anticipated in lung cancer and is likely to excite.

The large biotech, which typically hasn’t attracted top billing at the ASCO meeting, plans to host an investor event Monday night featuring AMG 510 as well as its pipeline of bispecific cancer therapies.

The company is already considering next steps for the targeted therapy. According to a federal database of clinical trials, Amgen’s Phase 1 study is set to enroll up to 60 patients, and the company plans to launch a registrational study in the future.

“We believe investigational AMG 510 has high potential as both a monotherapy and in combination with other targeted and immune therapies,” said Amgen’s R&D chief David Reese in a statement.

Amgen’s not the only one convinced KRAS might now be targeted. Mirati Therapeutics also has a KRAS G12C inhibitor now in clinical testing, with data set to read out later this year.