KRAS, one of can­cer’s tough­est tar­gets, sees a surge of new ther­a­pies try­ing to lim­it side ef­fects: #AACR23

OR­LAN­DO – Two years af­ter Am­gen won ap­proval for a drug go­ing af­ter one of can­cer’s most frus­trat­ing ge­net­ic tar­gets, re­searchers be­lieve they’re fi­nal­ly be­gin­ning to scratch the sur­face of the class’ po­ten­tial.

The tar­get, known as KRAS, is a pro­tein reg­u­lat­ing how cells grow and di­vide. Mu­ta­tions can cause the pro­tein to get stuck in the “on” po­si­tion, trig­ger­ing un­con­trolled ma­lig­nant cell growth. The first gen­er­a­tion of KRAS in­hibitors, which in­clude Am­gen’s Lumakras (so­tora­sib) and Mi­rati’s Kraza­ti (ada­gra­sib), tar­get a mu­ta­tion called G12C to lock the pro­tein in “off” mode.

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