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. Author manuscript; available in PMC: 2014 May 28.
Published in final edited form as: Nat Rev Cancer. 2011 Oct 24;11(11):775–791. doi: 10.1038/nrc3151

Table 2.

Clinical trials with FTIs*

Disease Phase Patients (median age) Clinical response and number of patients FT activity or prenylation Response rate (%) Other comments
Tipifarnib
Acute leukaemia I 34 (63) 2 CR and 8 PR FT ↓§ and HDJ2 ↓ 29.4 No NRAS mutations in patient tumours
Advanced bladder cancer II 34 (64) 2 PR and 13 SD ND 5.9 Response rate does not warrant further investigation
Advanced breast cancer II 76 (54) 9 PR and 9 SD ND 11.8 All responders had wild-type RAS genes
Advanced colon cancer II 55 (69) 1 PR, 11 SD, and 31 PD and MD ND 1.8 Tipifarnib is ineffective
Advanced NSCLC II 44 (71) 7 SD HDJ2 ↓ and prelamin A ↓. FT ↓ in 83% of patients 0 No objective response. Future studies should be done with combinations
Advanced solid tumours I 25 (58) 0 CR, 0 PR, 8 SD, and 17 PD and MD Data not shown 0 No objective response
Advanced solid tumours I 9 (53) 1 SD, and 8 PD and MD ND 0 No objective response
Advanced solid tumours I 28 (56) 2 PR and 3 SD ND 7.1 5 of 15 patients had KRAS mutations
Advanced solid tumours I 21 6 SD ND 0 No objective response. Phase II trial recommended
AML II 252 (62) 11 CR and 8 PR ND 7.5 MS for patients with CR: 369 days
AML II 145 (74) 22 CR, 3 PR, 50 SD and 58 PD and MD HDJ2 ↓ 17.2 Median duration of CR: 7.3 months
AML III 228 (76) 18 CR, 20 PR, 105 SD, and 36 PD and MD ND 16.7 MS: 107 days. 8% of patients had a CR with an MS of 666 days
229 0 CR, 3 PR, 130 SD, and 46 PD and MD 1.3 MS: 109 days
Brain tumours II 81 (11) 2 PR ND 2.5 Very little activity
CML, myelofibrosis and multiple myeloma 40 (57) 7 CR and 7 PR ND 17.5 Clinical activity in CML and myelofibrosis
Metastatic pancreatic cancer II 20 (61) 1 SD FT ↓ by 50% and HDJ2 ↓ by 33% 0 No objective response. MS: 19.7 weeks
Multiple myeloma II 36 (62) 0 CR, 0 PR, 23 SD, and 13 PD and MD FT ↓ and HDJ2 ↓ 0 No objective response. No correlation between FT ↓ and disease stabilization
MDS I 20 (66) 1 CR, 5 PR, and 1 PD and MD FT ↓ and HDJ2 ↓ 30 No correlation between FT ↓ and response. No correlation between RAS mutation status and response
MDS II 27 (66) 2 CR and 1 PR ND 11.1 Modest antitumour activity
MDS II 82 (67) 26 PR and 37 SD ND 31.7 Median duration of CR: 11.5 months
MDS I 61 (68) 3 CR and 13 PR FT ↓ by 75% 26.2 Only one responder with a KRAS mutation. No correlation between FT ↓ and dose
Neuro-fibromatosis and neurofibromas I 40 (≤15) FT ↓ by 43% and HDJ2 ↓ 0 No objective response
Pancreatic cancer II 53 (65) ND 0 No objective response. MS: 2.6 months
Small-cell lung cancer II 20 (62) 1 SD ND 0 No objective response. MS: 6.8 months. Progression-free MS: 1.4 months
Advanced colon cancer III 235 (61) 0 CR, 1 PR, 57 SD, and 155 PD and MD ND 0.4 MS: 174 days. SD >3 months: 24%
133 (62) 0 CR, 0 PR, 17 SD, and 107 PD and MD 0 MS: 185 days. SD >3 months: 13%
Lonafarnib
Advanced solid tumours I 24 (57) 0 CR, 0 PR and 2 SD ND 0 No objective response
Advanced solid tumours I 12 (61) 0 CR and 0 PR Prelamin A ↓ 0 No objective response
Advanced solid tumours I 22 (54) 1 CR and 1 PR FT ↓ 12.5# Sponsor terminated study early owing to negative interim efficacy. FT ↓ not correlated with response
Advanced solid tumours II 15 (57) 0 CR, 0 PR and 7 SD ND 0 No objective response
CML Pilot 13 (62) 0 CR and 2 PR ND 15.5
CNS tumours I 48 (12) 0 CR, 1 PR and 9 SD ND 2.1
Metastatic colon cancer II 21 (64) 0 CR, 0 PR and 3 SD ND 0 No objective response
MDS or sAML II 16 (70) 1 PR ND 6.7
NSCLC II 29 (58) 3 PR, 11 SD, and 15 PD and MD ND 10.3 MS: 39 months. Well-tolerated. Further clinical trials recommended
Refractory urothelial cancer (transitional cell carcinoma) II 10 (65) 0 CR, 0 PR, 2 SD, and 8 PD and MD Small HDJ2 ↓ 0 No objective response
Solid tumours I 20 (59) 1 PR and 8 SD Prelamin A ↓ 5.0
BMS-214662
Acute leukaemia I 30 (53) 4 CR and 1 PR Short-lived FT ↓ 16.7
Advanced solid tumours I 44 (54) 0 CR, 0 PR and 1 SD Transient FT ↓ by 89.5% 0 No objective response. One patient with pancreatic cancer survived for >3.5 years
Advanced solid tumours I 68 (60) 0 CR, 0 PR and 5 SD Short-lived FT ↓ 0 No objective response
Advanced solid tumours I 19 (55) 1 SD, and 18 PD and MD ND 0 No objective response
Solid tumours I 25 (57) 1 PR, 16 SR, and 8 PD and MD Short-lived FT ↓ 4.0 Response was minor

AML, acute myeloid leukaemia; CML, chronic myeloid leukaemia; CNS, central nervous system; CR, complete response; FNTB, farnesyltransferase β-subunit; FT, farnesyltransferase; FTIs, FT inhibitors; GGTI, geranylgeranyltransferase 1 inhibitor; HI, haematological improvement; MD, metastatic disease; MDS, myelodysplastic syndrome; MS, median survival; ND, not determined; NSCLC, non-small-cell lung cancer; OS, overall survival; PD, progressive disease; PR, partial response; sAML, secondary acute myeloid leukaemia; SD, stable disease.

*

See Supplementary information S4 (table) for a table with references. This table only considers FTIs because, to our knowledge, only one GGTI, GGTI-2418, is currently in clinical trials. Studies that did not evaluate tumour response are not included. Median ages are rounded to the closest integer. The number of evaluable patients is stated whenever possible. The response rate was calculated by dividing the sum of complete and partial responses by the number of evaluable patients.

PR includes haematological improvement.

§

Downward arrows indicate a reduction of enzyme activity (in the case of FT) or a reduction in farnesylation (in the case of HDJ2 or prelamin A).

This patient cohort received best supportive care.

In this study all patients received best supportive care, with 235 receiving tipifarnib and 133 receiving a placebo.

#

Number differs from the authors’ calculation as they included SD, resulting in a response rate of 37.5%.