Olutasidenib in combination with azacitidine induces durable complete remissions in patients with relapsed or refractory mIDH1 acute myeloid leukemia: a multicohort open-label phase 1/2 trial

Table 1 Patient demographic and baseline disease characteristics in the full analysis population

Parameter	Total (N = 67)
Age, median years (range)	66 (28–82)
< 65, n (%)	29 (43)
65 to < 75, n (%)	21 (31)
≥ 75, n (%)	17 (25)
Sex, n (%)
Male	36 (54)
Female	31 (46)
Race, n (%)
Asian	3 (4)
Black	4 (6)
White	39 (58)
Not reported	21 (31)
Region, n (%)
North America	32 (48)
EU	29 (43)
Asia Pacific	6 (9)
ECOG performance status score, n (%)^b
0	23 (34)
1	32 (48)
2	12 (18)
Prior number of regimens, n (%)^c
1	11 (16)
2	25 (37)
3 or more	31 (46)
Prior induction^d	67 (100)
Prior venetoclax treatment	4 (6)
Prior HMA treatment, n (%)^e	27 (40)
Prior IDH1i therapy, n (%)	21 (31)
Prior olutasidenib therapy, n (%)	16 (24)
Prior HSCT, n (%)	7 (10)
AML type, n (%)
Primary de novo	44 (66)
Secondary	23 (34)
AML cytogenetic risk category, n (%)^f
Favorable	0
Intermediate	48 (72)
Poor	12 (18)
Unknown/Missing	7 (10)
Hematologic laboratory parameters, median (range)
Percentage of bone marrow blasts	50 (4, 98)
Percentage of peripheral blood blasts	60 (1, 97)
White blood cells × 10⁹/L	2.3 (0, 90.7)
Absolute neutrophil count × 10⁹/L	0.41 (0, 17.2)
Renal function (creatinine clearance), n (%)
Normal (≥ 90 mL/min)	36 (54)
Mildly impaired (60–89 mL/min)	22 (33)
Moderately impaired (30–59 mL/min)	9 (13)
Severely impaired (15–29 mL/min)	0
AML IDH1 mutation type, n (%)^g
R132C	40 (60)
R132H	19 (28)
R132G/L/S	8 (12)
AML number of co-mutations, n (%)
None	6 (9)
1 to 3	39 (58)
4 to 10	13 (19)
Unknown	9 (13)
Co-mutations in > 10% overall patients, n (%)
DNMT3A	22 (33)
NPM1	18 (27)
FLT3	13 (19)
SRSF2	9 (13)
ASXL1	9 (13)

^aPatient did not identify as American Indian or Alaskan Native, Asian, Black or African American, Native Hawaiian or other Pacific Islander
^bThere were no patients with ECOG performance status score of 3 or 4
^cMost common (> 5% of total patients) prior treatments included cytarabine (81%), idarubicin (36%), daunorubicin (30%), fludarabine (30%), investigational antineoplastic drugs (27%), azacitidine (25%), decitabine (16%), granulocyte colony stimulating factor (12%), midostaurin (10%), busulfan (9%), ivosidenib (7%), venetoclax 6%)
^d2 patients (3%) had missing regimen type in the medical history provided by the investigator; however, both patients had azacitidine as their induction regimen
^eOf the 27 patients with prior HMA treatment, 17 had azacitidine, 11 had decitabine, 1 had guadecitabine; there was an overlap of 2 patients who had both prior azacitidine and prior decitabine
^fCytogenetic risk was assessed by investigators, according to National Comprehensive Cancer Network (NCCN) Clinical Practice Guidelines for AML or European Leukemia Network guidelines
^gMutation type as reported by investigator

ISSN: 1756-8722