Pleiotropic ABC efflux transporter that transports and confers resistance to structurally and functionally unrelated compounds including rhodamine 6G, Nile red, caspofungin, cycloheximide, or azoles such as fluconazole, itraconazole, ketoconazole, posaconazole, voriconazole, and isavuconazole (PubMed:10543759, PubMed:12244114, PubMed:15105111, PubMed:15105136, PubMed:15388433, PubMed:15498768, PubMed:16803598, PubMed:17581937, PubMed:18591262, PubMed:20038613, PubMed:20450660, PubMed:21134356, PubMed:21408004, PubMed:22788839, PubMed:26482310, PubMed:27486188, PubMed:29371812, PubMed:29784839). Chlorbromuron, itraconazole, yohimbine, ketoconazole, miconazole, clotrimazole, DE-11, tamoxifen, quinidine, verapamil can compete for rhodamine 6G's binding site(s) while compounds such as propanil, chloramphenicol, benomyl, voriconazole, tritylimidazole, ketoconazole, miconazole, tamoxifen, gefitinib shared binding site(s) with fluconazole. Nile red mediated efflux appears to be relatively more specific since only five compounds such as ZW3-12, rhodamine 123, miconazole, clotrimazole, and itraconazole can inhibit its accumulation (PubMed:21134356). Does not use as substrates 4-nitroquinoline 1-oxide (4-NQO) and disulfiram (PubMed:21134356). Does not play a role in the azole resistance in mature biofilms (PubMed:18651314). Inhibited by clorgyline (PubMed:22203607). Inhibited by RC21v3, a 4-methoxy-2,3,6-trimethylbenzenesulphonyl derivative of the D-octapeptide D-FFKWQRRR, via the interaction with the ectodomain (PubMed:22788839). FK506, enniatin, milbemycin alpha-11, and milbemycin beta-9 also inhibit CDR1 activity (PubMed:22788839). Inhibited by milbemycin A3/A4 oxim derivatives (PubMed:23208712, PubMed:24838041). Azole exposure induced expression 4- to 12-fold via regulation by the transcription factor PDR1 that stimulates gene expression via binding to elements called pleiotropic drug response elements (PDREs) (PubMed:12458010, PubMed:10543759, PubMed:16803598, PubMed:21193550, PubMed:21408004, PubMed:23979762, PubMed:24645630, PubMed:19148266, PubMed:21131438, PubMed:29464833). Expression is highly up-regulated in azole-resistant isolates (PubMed:10543759, PubMed:16735426, PubMed:16891541, PubMed:17158937, PubMed:17581937, PubMed:18591262, PubMed:18782778, PubMed:19380598, PubMed:19196495, PubMed:20038613, PubMed:20450660, PubMed:21134356, PubMed:25818698, PubMed:27486188, PubMed:28894714, PubMed:29371812, PubMed:29784839). Loss of mitochondrial functions leads to increased expression (PubMed:21321146). Expression is temporary increased during the intermediate phase of biofilm development (PubMed:18651314). Expression is down-regulated by the transcription factor STB5 (PubMed:23229483). Expression is negatively regulated by the transcription factor JJJ1 via inactivation of the PDR1 transcriptional pathway (PubMed:29507891). Expression is also decreased by amphotericin B in voriconazole-resistant strains (PubMed:21282443). Phosphorylated at Ser-307 and Ser-484. Ser-307 and Ser-484 are dephosphorylated on glucose depletion and independently rephosphorylated during glucose exposure or under stress. Leads to susceptibility to the antifungal azole derivatives in azole-resistant clinical isolates (PubMed:10543759, PubMed:16803598). Suppresses the development of high-frequency azole resistance (HFAR) in a medium containing fluconazole (PubMed:11257032). Belongs to the ABC transporter superfamily.