For decades, sci­en­tists scratched their heads about KRAS, the no­to­ri­ous can­cer-caus­ing pro­tein. Its smooth ter­rain long elud­ed ma­nip­u­la­tion, large­ly due to the ab­sence of a dis­tinct pock­et for a drug to latch on to. How­ev­er, the process of tri­al and er­ror fi­nal­ly yield­ed progress — trig­ger­ing a flock of com­pa­nies, in­clud­ing Am­gen, J&J, Mer­ck, and As­traZeneca, to en­gi­neer com­pounds de­signed to an­nex the oft’ mu­tat­ed onco­gene. And now, it looks like Ger­many’s Boehringer In­gel­heim has of­fi­cial­ly en­tered the fold.

The first KRAS pock­et es­tab­lished by Am­gen $AMGN for at­tack is G12C, al­though small­er ri­val Mi­rati $MRTX is at the large drug­mak­er’s heels. The KRAS G12C mu­ta­tion is found in rough­ly 14% of non-small cell lung can­cer (NSCLC) pa­tients and 5% of col­orec­tal can­cer pa­tients, who are large­ly pre­sent­ed with a poor prog­no­sis and tend to be re­sis­tant to stan­dard ther­a­pies.

On Tues­day, Ever­core ISI’s Umer Raf­fat point­ed out that Boehringer now has a clin­i­cal-stage KRAS in­hibitor in its ar­se­nal. And un­like Am­gen and Mi­rati, the Ger­man drug­mak­er’s ap­proach is a pan-KRAS in­hibitor that hits SOS1 as well as G12C. SOS1 is a pro­tein that turns KRAS from an “off” to “on” state.

Am­gen’s keen­ly watched AMGN510 made a splash at the AS­CO con­fer­ence this year af­ter a small, ear­ly study showed five out of 10 pa­tients suf­fer­ing from ad­vanced, drug-re­sis­tant NSCLC saw a par­tial re­sponse to the ex­per­i­men­tal treat­ment, in­clud­ing one who went on to achieve a com­plete re­sponse af­ter the da­ta cut­off point. Last month, those da­ta were up­dat­ed at the World Con­fer­ence on Lung Can­cer. Re­searchers tracked a 54% par­tial tu­mor re­sponse, and ob­served tu­mors shrink­ing in sev­en of 13 NSCLC pa­tients.

An­a­lysts have been in­tox­i­cat­ed with the po­ten­tial of the com­pound for this cat­e­go­ry of heav­i­ly treat­ed pa­tients with few op­tions at their dis­pos­al — and have al­ready fore­cast the drug will gen­er­ate bil­lions in peak sales, should it se­cure ap­proval.

But over the week­end at the ES­MO meet­ing in Barcelona, en­thu­si­asm for the drug out­side of lung can­cer damp­ened, af­ter Am­gen un­veiled da­ta from the tranche of col­orec­tal can­cer pa­tients. Re­searchers re­port­ed a sin­gle par­tial re­sponse among 12 col­orec­tal can­cer pa­tients.

Mean­while, Mi­rati’s Phase I/II da­ta em­a­nat­ing from its ex­per­i­men­tal drug, MRTX849, for ad­vanced sol­id tu­mors that har­bor KRAS G12C mu­ta­tions are ex­pect­ed in the fourth quar­ter. The lit­tle biotech has tied up with No­var­tis — and the two are look­ing at com­bin­ing the G12C drug with a ther­a­py that tar­gets SHP2, which func­tions as a key reg­u­la­tor of cell cy­cle con­trol.

Rev­o­lu­tion Med­i­cines has the same po­ten­tial com­bo in-house. Oth­er KRAS con­tenders in­clude Mod­er­na $MR­NA and Mer­ck’s $MRK mR­NA-5671; J&J’s $JNJ col­lab­o­ra­tion with Well­spring on ARS-3248, a G12C tar­get­ed small mol­e­cule; and AZD4785, li­censed by As­traZeneca $AZN from Io­n­is — al­though the com­pound has been dis­con­tin­ued af­ter a poor show­ing in clin­i­cal tri­als.

In Au­gust, Boehringer tied up with MD An­der­son in­ves­ti­ga­tors in Hous­ton to cre­ate a joint “vir­tu­al re­search and de­vel­op­ment cen­ter” look­ing at two pop­u­lar prospects: KRAS in­hi­bi­tion and a TRAILR2 ag­o­nis­tic an­ti­body for apop­to­sis.

As an onco­gene, KRAS has the po­ten­tial to ren­der nor­mal cells can­cer­ous. Akin to HRAS and NRAS, it be­longs to the RAS fam­i­ly of onco­genes and plays a key role in cell di­vi­sion, cell dif­fer­en­ti­a­tion, and apop­to­sis.

The researcher behind base-editing is out with what some scientists are hailing as the biggest advancement in CRISPR technology since that 2016 breakthrough: “prime editing.” The new molecular gadget is capable of erasing any base pair and stenciling in another and cutting or adding long segments of DNA without breaking both strands of the helix.

David Liu, base editing pioneer and founder of Beam Therapeutics, published the findings in Nature alongside Andrew Anzalone. They estimated that the breakthrough “in principle” puts 89% of human diseases in purview — although experts cautioned that human therapies were a long way off.

For the past three years Frazier Healthcare Partners’ Bhaskar Chaudhuri has been carefully and quietly grooming Arcutis Therapeutics, a new dermatology play he co-founded to deliver topical formulations of well-known drugs. Now that the biotech is poised to enter Phase III, he’s being joined by a marquee syndicate for its $94.5 million Series C.

HBM Healthcare Investments, Vivo Capital, BlackRock, Omega Funds, Pivotal BioVentures, and Goldman Sachs jumped on board, joining Bain Capital Life Sciences, OrbiMed and RA Capital Management in backing Arcutis’ lead topical cream for plaque psoriasis.

The remedy for the most common side effect for one of the most common multiple sclerosis drugs is simple: aspirin.

Taking aspirin with Biogen’s Tecfidera will reduce the flush, a sometimes painful form of red skin irritation, many patients experiences. The problem is that the aspirin has to be taken at least 30 minutes before Tecfidera, turning a simple twice-a-day, one-dose oral drug into a staggered two-drug regimen.

Despite a head start, when Bristol-Myers Squibb and its pioneering checkpoint inhibitor Opdivo suffered a key lung cancer setback in 2016, they found themselves relegated to the backseat as Merck’s Keytruda seized the wheel on the road to immunotherapy stardom. Bristol-Myers has since suffered blow after blow in its quest to take a big slice of the lucrative market, peppered with some small successes. On Tuesday, the New Jersey drugmaker touted positive data from a Phase III open-label study in a bid to carve itself a piece of the frontline lung cancer market.