Selecting First-line Therapy in the EGFR Mutant NSCLC Setting NSCLC, non-small-cell lung cancer. This program is supported by an educational grant from Boehringer Ingelheim.

Faculty Everett Vokes, MD John E. Ultmann Professor Chair, Department of Medicine Physician-in-Chief The University of Chicago Medicine and Biological Sciences Chicago, Illinois Everett Vokes, MD, has disclosed that he has received consulting fees from Amgen, AstraZeneca, Boehringer Ingelheim, Celgene, Genentech, Lilly, Merck, Synta, and VentiRx.

Background EGFR mutation recognized as major determinant of response to EGFR TKIs Mutation frequency approximately 10% to 30% of NSCLC First-, second-, and third-generation drugs available Not all mutations equally associated with response Resistance patterns well described NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. Slide credit: clinicaloptions.com Stewart EL, et al. Transl Lung Cancer Res. 2015;4:67-81.

EGFR Mutations in NSCLC 9% exon 20 variants 3% codon 719 variants 2% other variants 40% L858R substitution 46% exon 19 deletions NSCLC, non-small-cell lung cancer. Herbst RS, et al. N Engl J Med. 2008;359:1367-1380. Sequist LV, et al. J Clin Oncol. 2007;25:587-595 Slide credit: clinicaloptions.com

Screening for EGFR Mutations Parameter Direct DNA (Sanger) Sequencing Next-Generation Sequencing DNA source Tissue from biopsy/resection Tissue, blood/plasma, urine Sensitivity Low: mutant variant must be ≥ 20% of sample to be detectable High: mutant variant can be as low as 5% of input sample Specificity High High (equivalent to Sanger) Turnaround time Within 10 working days of receipt Up to several wks Advantages Gold standard: well defined, readily available methodology High throughput; simultaneously test multiple targets/genes of interest; quantitative; decreased cost per bp Limitations Tumor tissue samples often too small or heterogeneous; low throughput; limited in detecting gene copy number changes Clinical standards not yet established; complex workflow and analysis bp, base pair Khoo C, et al. Transl Lung Cancer Res. 2015;4:126-141.Lindeman NI, et al. J Thorac Oncol. 2013;8:823-859. Luthra R, et al. Cancers. 2015;7:2023-2036. Rizzo JM, et al. Cancer Prev Res. 2012;5:887-900. Chin EL, et al. BMC Genet. 2013;14:6. Slide credit: clinicaloptions.com

Lung Cancer Mutation Consortium: Single Driver Mutations in NSCLC No mutation detected ERBB2 3% KRAS 25% MET AMP < 1% EGFR 17% MEK1 < 1% EML4-ALK 8% NRAS < 1% Double mutants 3% AKT1 0% BRAF 2% PIK3CA < 1% Mutations found in 64% (466/733) of tumors completely tested NSCLC, non-small-cell lung cancer. Slide credit: clinicaloptions.com Kris MG, et al. JAMA. 2014;311:1998-2006.

EGFR Mutations: Context Found in approximately 10% to 30% of pts with NSCLC More common in neversmokers, adenocarcinomas, females, Asians Associated with response to first-, second-, and third-generation TKIs Predominantly located in EGFR exons 18-21 85% of EGFR mutations are either deletions in exon 19 or a single-point mutation in exon 21 (L858R) The specific EGFR mutation identified is important There are sensitive mutations, primary resistance mutations (often exon 20), and acquired resistance mutations (T790M) NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. Stewart EL, et al. Transl Lung Cancer Res. 2015;4:67-81. Chan BA, et al. Transl Lung Cancer Res. 2015;4:36-54. Slide credit: clinicaloptions.com

IPASS: First-line Gefitinib vs Paclitaxel/ Carboplatin in Stage IIIB/IV NSCLC Open-label phase III trial Primary endpoint: PFS Secondary endpoints: OS, ORR, quality of life, symptom reduction, safety Study conducted in Asian countries Up to six 3-wk cycles Gefitinib 250 mg/day PO (n = 609) Previously untreated pts with stage IIIB/IV NSCLC, adenocarcinoma, never or ex-light smokers, WHO PS 0-2 (N = 1217) Paclitaxel 200 mg/m2 IV on Day 1 + Carboplatin AUC 5-6 mg/mL/min IV on Day 1 (n = 608) AUC, area under the curve; NSCLC, non-small-cell lung cancer; PS, performance status; WHO, World Health Organization. Slide credit: clinicaloptions.com Mok TS, et al. N Engl J Med. 2009;361:247-257.

Gefitinib vs Paclitaxel/Carboplatin in Advanced NSCLC: PFS by EGFR Status PFS: gefitinib superior to carboplatin/paclitaxel in ITT population HR for progression/death: 0.74 (95% CI: 0.65-0.85; P < .001) EGFR mutations strongly predicted PFS (and tumor response) to first-line gefitinib vs carboplatin/paclitaxel EGFR Mutation Positive EGFR Mutation Negative 1.0 1.0 Gefitinib Pac/carbo Gefitinib Pac/carbo 0.8 0.8 HR: 0.48 (95% CI: 0.36-0.64; P < .001) HR: 2.85 (95% CI: 2.05-3.98; P < .001) 0.6 Carbo, carboplatin; ITT, intent to treat; NSCLC, non-small-cell lung cancer; Pac, paclitaxel. 0.6 Probability of PFS Probability of PFS 0.4 0.4 0.2 0.2 4 8 12 16 20 24 4 8 12 16 20 24 Mos Since Randomization Mos Since Randomization Slide credit: clinicaloptions.com Mok TS, et al. N Engl J Med. 2009;361:947-957.

Mos From TKI Initiation EGFR TKIs in EGFR-Mutant Metastatic Lung Adenocarcinoma: 5-Yr PFS and OS Pts (N = 137) treated with erlotinib or gefitnib were included PFS OS 1.0 1.0 0.8 0.8 0.6 0.6 Probability of PFS Median PFS: 12.1 mos Probability of OS Median OS: 30.9 mos 0.4 0.4 EGFR, epidermal growth factor receptor; NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. 0.2 0.2 10 20 30 40 50 60 20 40 60 80 Mos From TKI Initiation Mos From Treatment Initiation Slide credit: clinicaloptions.com Lin JJ, et al. J Thorac Oncol. 2016;11:556-565.

Stratified by mutation type,* ECOG PS (0 vs 1 vs 2) EURTAC: Erlotinib vs Chemo in EGFR Mutation–Positive, Stage IIIB/IV NSCLC Randomized, open-label phase III trial Stratified by mutation type,* ECOG PS (0 vs 1 vs 2) Erlotinib 150 mg/day (n = 86) PD Pts with no prior chemotherapy, stage IIIB/IV NSCLC, mutated EGFR,* ECOG PS 0-2 (N = 174†) Platinum Doublet‡ Q3W x 4 cycles (n = 87) PD Primary endpoint: PFS (interim analysis planned at 88 events) Secondary endpoints: ORR, OS, location of progression, safety, EGFR-mutation analysis, QoL AUC, area under the curve; ECOG, Easter Cooperative Oncology Group; NSCLC, non-small-cell lung cancer; PD, progressive disease; PS, performance status; QoL, quality of life. *Exon 19 deletion or exon 21 L858R mutation. †1227 pts screened; 174 pts with mutated EGFR enrolled; 1 pt withdrawn. ‡Cisplatin 75 mg/m2 Day 1/docetaxel 75 mg/m2 Day 1; cisplatin 75 mg/m2 Day 1/ gemcitabine 1250 mg/m2 Days 1, 8; carboplatin AUC = 6 Day 1/docetaxel 75 mg/m2 Day 1; carboplatin AUC = 5 Day 1/gemcitabine 1000 mg/m2 Days 1, 8. Slide credit: clinicaloptions.com Rosell R, et al. Lancet Oncol. 2012;13:239-246.

PFS in ITT Population 1.0 Erl (n = 86) 0.8 Chemotherapy (n = 87) 0.6 0.4 0.2 Erl (n = 86) Chemotherapy (n = 87) HR: 0.37 (95% CI: 0.25-0.54; log-rank P < .0001) Probability of PS 5.2 9.7 Erl, erlotinib; ITT, intent to treat. 0 3 6 9 12 15 18 21 24 27 30 33 Mos Pts at Risk, n Erl 86 63 54 32 21 17 9 7 4 2 2 0 Chemo 87 49 20 8 5 4 3 1 0 0 0 0 Slide credit: clinicaloptions.com Rosell R, et al. Lancet Oncol. 2012;13:239-246.

First-line Treatment With EGFR TKIs vs Chemotherapy in EGFR-Mutated NSCLC Study Treatment N Median PFS, Mos Median OS, Mos Maemondo[1] Gefitinib vs carboplatin/ paclitaxel 230 10.8 vs 5.4 (P < .001) 30.5 vs 23.6 (P = .31) Mitsudomi[2,3] Gefitinib vs cisplatin/docetaxel 172 9.2 vs 6.3 (P < .0001) 35.5 vs 38.8 (HR: 1.19) OPTIMAL[4,5] Erlotinib vs carboplatin/gemcitabine 165 13.1 vs 4.6 22.8 vs 27.2 EURTAC[6] platinum-based chemotherapy 174 9.7 vs 5.2 19.3 vs 19.5 (P = .87) LUX-Lung 3[7,8] Afatanib vs cisplatin/pemetrexed 345 11.1 vs 6.9 (P = .001) 28.2 vs 28.2 (P = .39) LUX-Lung 6[8,9] Afatinib vs cisplatin/gemcitabine 364 11.0 vs 5.6 23.1 vs 23.5 (P = .61) NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. 1. Maemondo M, et al. N Engl J Med. 2010;362:2380-2388. 2. Mitsudomi T, et al. Lancet Oncol. 2010;11:121-128. 3. Mitsudomi T, et al. ASCO 2012. Abstract 7521. 4. Zhou C, et al. Lancet Oncol. 2011;12:735-742. 5. Zhou C, et al. Ann Oncol. 2015;26:1877-1883. 6. Rosell R, et al. Lancet Oncol. 2012;13:239-246. 7. Sequist LV, et al. J Clin Oncol. 2013;31:3327-3334. 8. Yang JC, et al. Lancet Oncol. 2015;16:141-151. 9. Wu YL, et al. Lancet Oncol. 2014;15:213-222. Slide credit: clinicaloptions.com 13

Meta-analysis of Randomized First-line EGFR TKI Studies: Improved PFS HR (95% CI) HR (95% CI) Study EGFRmut (first-line therapy) EURTAC First-SIGNAL GTOWG INTACT1-2 IPASS LUX LUNG3 NEJ002 OPTIMAL TALENT TOPICAL TRIBUTE WJTOG3405 Subtotal 0.37 (0.25-0.54) 0.54 (0.27-1.10) 1.08 (0.24-4.90) 0.55 (0.19-1.60) 0.48 (0.36-0.64) 0.58 (0.43-0.78) 0.32 (0.24-0.44) 0.16 (0.11-0.26) 0.59 (0.21-1.67) 0.90 (0.39-2.06) 0.49 (0.20-1.20) 0.52 (0.38-0.72) 0.43 (0.38-0.49) TKI, tyrosine kinase inhibitor. Favors EGFR TKI Favors Chemo Slide credit: clinicaloptions.com Lee CK, et al. J Natl Cancer Inst. 2013;105:595-605.

3 Generations of EGFR TKIs T790M Erlotinib T790M EGFRm Wt 100x Afatinib Osimertinib EGFRm T790M Wt 10x Relative IC50 Wt m, mutated; TKI, tyrosine kinase inhibitor; Wt, wild type. 1x EGFRm Gefitinib Li D, et al. Oncogene. 2008;27:4702-4711. Ranson M, et al. WCLC 2013. Abstract MO21.12. Moyer JD, et al. Cancer Res. 1997;57:4838-4848. Kancha RK, et al. Clin Cancer Res. 2009;15:460-467. Slide credit: clinicaloptions.com 15

LUX-Lung 2: High Response of EGFR-Mutated, TKI-Naive NSCLC to Afatinib Phase II: 61% (79/129) pts achieved ORR (2 CR; 77 PR) regardless of type of EGFR mutation Measurable Tumor at Time of Best Response 50 20 Maximum Decrease From Baseline(%) -30 NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. -50 -100 20 40 60 80 100 Pt Slide credit: clinicaloptions.com Yang JC, et al. Lancet Oncol. 2012;13:539-548.

Cisplatin/Pemetrexed (n = 104) LUX-Lung 3: Afatinib vs Chemo Improves PFS in TKI-Naive EGFR-Mutated NSCLC Phase III study of afatinib vs cisplatin-pemetrexed in EGFR-mutant NSCLC adenocarcinoma (N = 345) Median PFS by del(19) and L858R EGFR Mutation Status Afatinib (n = 204) Cisplatin/Pemetrexed (n = 104) 1.0 Events, n (%) Median, mos 130 (64) 13.6 61 (59) 6.9 0.8 Afatinib Cisplatin/pemetrexed 0.6 Probability of PFS (HR: 0.47; 95% CI: 0.34-0.65; P < .001) 0.4 NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. 0.2 3 6 9 12 15 18 21 24 27 Mos Slide credit: clinicaloptions.com Sequist LV, et al. J Clin Oncol. 2013;31:3327-3334. Sequist et al, JCO, 2013

Estimated OS Probability Estimated OS Probability LUX-Lung 3+6: OS by del(19) and L858R Mutation Status for Afatinib vs Cisplatin/Pemetrexed del(19) Afatinib (n = 236) Chemo (n = 119) Median, mos 31.7 20.7 HR (95% CI) 0.59 (0.45-0.77) P = .0001 L858R Afatinib (n = 183) Chemo (n = 93) Median, mos 22.1 26.9 HR (95% CI) 1.25 (0.92-1.71) P = .1600 1.0 1.0 0.8 0.8 0.6 0.6 Estimated OS Probability Estimated OS Probability 0.4 0.4 0.2 0.2 0 6 12 18 24 30 36 42 48 0 6 12 18 24 30 36 42 48 Mos Mos Slide credit: clinicaloptions.com Yang JC, et al. Lancet Oncol. 2015;16:141-151.

Is OS With Afatinib in LUX-Lung 3/6 Superior to That of Other EGFR TKIs? 45 EGFR TKI Chemo 40 35 30 25 Median OS (Mos) 20 15 10 5 TKI, tyrosine kinase inhibitor. Mitsudomi (N = 172) Maemondo (N = 230) EURTAC (N = 174) OPTIMAL (N = 165) LUX-Lung-3 (N = 345) LUX-Lung-6 (N = 364) Terminated early after interim analysis? Gefitinib Erlotinib Afatinib Mitsudomi T, et al. Lancet Oncol. 2010;11:121-128. Maemondo M, et al. N Engl J Med. 2010;362:2380-2388. Rosell R, et al. Lancet Oncol. 2012;13:239-246. Zhou, et al. Lancet Oncol. 2011;12:735-742. Yang JC, et al. Lancet Oncol. 2015;16:141-151. Slide credit: clinicaloptions.com

LUX-Lung 2+3+6: Afatinib in NSCLC Pts With Uncommon EGFR Mutations Combined post hoc, ITT analysis of data on pts with uncommon EGFR mutations (n = 100) prospectively collected from the LUX-Lung 2, 3, and 6 trials Afatinib: n = 75; chemotherapy: n = 25 Pts with uncommon EGFR mutations given afatinib categorized into 3 cohorts Cohort n Uncommon Mutations Group 1 38 Point mutations or duplications in exons 18-21 (L861Q, G719S, G719A, G719C, S768I, rare others) alone or in combination with each other Group 2 14 De novo T790M mutations in exon 20 alone or in combination with other mutations Group 3 23 Exon 20 insertions ITT, intent to treat; NSCLC, non-small-cell lung cancer. Slide credit: clinicaloptions.com Yang JC, et al. Lancet Oncol. 2015;16:830-838.

Afatinib in NSCLC Pts With Uncommon EGFR Mutations: Tumor Shrinkage Decreases in tumor size in response to afatinib associated with an increase in PFS Tumor Shrinkage and PFS 120 40 100 Group 1 Group 2 Group 3 35 30 80 25 60 20 PFS (Mos) 15 40 10 Maximum Decrease From Baseline (%) 20 5 -20 NSCLC, non-small-cell lung cancer. -40 -60 -80 -100 5 10 15 20 25 30 35 40 45 50 55 60 65 70 Pt Index Sorted by Maximum % Decrease in Descending Order Slide credit: clinicaloptions.com Yang JC, et al. Lancet Oncol. 2015;16:830-838.

Afatinib in NSCLC Pts With Uncommom EGFR Mutations: Response Outcome Afatinib Group 1 (n = 38)* Afatinib Group 2 (n = 14)†‡ Group 3 (n = 23)‡ Chemotherapy Group (n = 25)§ ORR, % (95% CI) 71.1 (54.1-84.6) 14.3 (1.8-42.8) 8.7 (1.1-28.0) 24 (9.4-45.1) Median DOR, mos (95% CI) 11.1 (4.1-15.2) 8.2 (4.1-12.4) 7.1 (4.2-10.1) -- Disease control, % (95% CI) 84.2 (68.7-94.0) 64.3 (35.1-87.2) 65.2 (42.7-83.6) Median PFS, mos (95% CI) 10.7 (5.6-14.7) 2.9 (1.2-8.3) 2.7 (1.8-4.2) (5.2-10.8) Median OS, mos (95% CI) 19.4 (16.4-26.9) 14.9 (8.1-24.9) 9.2 (4.1-14.2) 30.2 (13.0-42.3) DOR, duration of response; NSCLC, non-small-cell lung cancer. *Consists of pts with all point mutations or duplications in exons 18-21. †Consists of pts with de novo T790M mutations. ‡Consists of pts with exon 20 insertions. §Consists of pts with mutations falling into groups 1/2/3 (n = 18/3/2). For chemotherapy cohort, median PFS/median OS longer for pts in group 1 (8.4/40.8 mos) vs pts in groups 2 (6.7/22.2 mos) or 3 (5.2/31.0 mos) Slide credit: clinicaloptions.com Yang JC, et al. Lancet Oncol. 2015;16:830-838.

LUX-Lung 7: PFS With First-line Afatinib vs Gefitinib in EGFR-Mutated NSCLC 100 80 Afatinib Gefitinib HR: 0.73 (95% CI: 0.57-0.95; P = 0.017) 60 PFS (%) 40 20 NSCLC, non-small-cell lung cancer. 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Mos Pts at Risk, n Afatinib Gefitinib 160 159 142 132 112 106 94 83 67 52 47 22 34 14 27 9 21 7 13 5 6 3 3 3 1 1 0 1 0 0 Slide credit: clinicaloptions.com Park K, et al. Lancet Oncol. 2016;[Epub ahead of print].

Estimated Probability of Being on Treatment (%) LUX-Lung 7: Time-to-Treatment Failure With First-line Afatinib vs Gefitinib 100 80 Afatinib Gefitinib HR: 0.73 (95% CI: 0.58-0.92; P = .0073) 60 Estimated Probability of Being on Treatment (%) 40 20 NSCLC, non-small-cell lung cancer. 3 6 9 12 15 18 21 24 27 30 33 36 39 42 Mos Pts at Risk, n Afatinib Gefitinib 160 159 148 144 133 120 113 103 91 74 68 59 56 43 48 30 40 21 25 11 18 6 9 6 5 2 0 2 0 0 Slide credit: clinicaloptions.com Park K, et al. Lancet Oncol. 2016;[Epub ahead of print].

Mos From Treatment Initiation Mos From Treatment Initiation 5-Yr OS in EGFR-Mutated NSCLC Treated With Either Erlotinib or Gefitinib Prolonged survival associated with exon 19 vs exon 18 or 21 deletions No extrathoracic mets (n = 79) Extrathoracic mets (n = 58) 1.0 1.0 Exon 18 (n = 4) Exon 19 (n = 76) Exon 21 (n = 21) 0.8 0.8 0.6 0.6 Median OS: 26.7, 41.4 Median OS: 23.9, 33.6, 27.0 Probability of OS Probability of OS 0.4 HR: 0.55 (P = .001) 0.4 HR: 0.52 (P = .001) 0.2 0.2 NSCLC, non-small-cell lung cancer. 20 40 60 80 20 40 60 80 Mos From Treatment Initiation Mos From Treatment Initiation Slide credit: clinicaloptions.com Lin JJ, et al. J Thorac Oncol. 2016;11:556-565.

Toxicity of EGFR TKIs in NSCLC Study Treatment-Related AEs, % Diarrhea Rash Paronychia Stomatitis Gr 1/2 Gr 3/4 Gefitinib Mitsudomi Maemondo 47 38 1.1 0.9 72 75 2.3 5.3 27 NR 1.2 2.6 19 11 Erlotinib OPTIMAL EURTAC 21 44 1 5 48 56 2 12 3 10 Afatinib LUX-Lung 3 LUX-Lung 6 80 81 14.4 5.4 65 16.2 14.6 45 32 11.4 63 8.7 AE, adverse event; Gr, grade; NR, not reported; NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. Gefitinib and erlotinib have comparable toxicity Afatinib associated with more severe toxicity than gefitinib or erlotinib Slide credit: clinicaloptions.com Burotto M, et al. Oncologist. 2015;20:400-410.

First-line Erlotinib ± Carboplatin/Paclitaxel in EGFR-Mutated NSCLC CALGB trial of first-line combination therapy in clinically selected pts (N = 181) 40% (66 of 164 evaluable pts) had EGFR mutations PFS OS 1.0 1.0 E (n = 33) ECP (n = 33) E (n = 33) ECP (n = 33) 0.8 0.8 0.6 0.6 Proportion Progression Free Probability of OS 0.4 0.4 0.2 0.2 HR: 0.77 (95% CI: 0.45-1.33; log-rank P = .3490) HR: 0.97 (95% CI: 0.49-1.91; log-rank P = .9227) C, carboplatin; E, erlotininb; Gr, grade; NSCLC, non-small-cell lung cancer; P, paclitaxel. 6 12 18 24 30 36 42 6 12 18 24 30 36 42 48 54 60 Mos Mos Addition of chemotherapy only served to increase toxicity Gr 3/4 hematologic: 2% vs 49%; Gr 3/4 nonhem: 24% vs 52%; P < .001 Slide credit: clinicaloptions.com Jänne PA, et al. J Clin Oncol. 2012;30:2063-2069.

Phase II Study: Erlotinib ± Bevacizumab in Advanced NSCLC With EGFR Mutations Erlotinib 150 mg QD + Bevacizumab 15 mg/kg q3w (n = 77) Pts with chemo-naive, nonsquamous NSCLC and EGFR mutations (del 19, L858R), no brain mets (N = 154) Treat until disease progression or unacceptable toxicity Erlotinib 150 mg QD (n = 77) Open-label study Primary endpoint: PFS (independent review; RECIST) Secondary endpoints: OS, tumor response, QoL, safety NSCLC, non-small-cell lung cancer; QoL, quality of life; RECIST, Response Evaluation Criteria In Solid Tumors. Seto T, et al. Lancet Oncol. 2014;15:1236-1244. Kato T, et al. ASCO 2014. Abstract 8005. Slide credit: clinicaloptions.com

Erlotinib ± Bevacizumab in Advanced NSCLC With EGFR Mutations: PFS EB E Median PFS, mos 16.0 9.7 HR (95% CI) 0.54 (0.36-0.79) P value .0015 1.0 0.8 0.6 EB E Probability of PFS 0.4 0.2 B, bevacizumab; E, erlotinib; NSCLC, non-small-cell lung cancer; PFS, progression-free survival. 9.7 16.0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 Mos Pts at Risk, n EB 75 72 69 64 60 53 49 38 30 20 13 8 4 4 E 77 66 57 44 39 29 24 21 18 12 10 5 2 1 Seto T, et al. Lancet Oncol. 2014;15:1236-1244. Kato T, et al. ASCO 2014. Abstract 8005. Slide credit: clinicaloptions.com

Summary of First-line EGFR TKIs in EGFR- Mutated NSCLC Erlotinib, gefitinib, and afatinib improve PFS and QoL Active in pts with poor PS Afatinib PFS superior to first-generation EGFR TKIs Choice of a specific EGFR TKI should consider toxicities and pt preferences Combination with bevacizumab under investigation NSCLC, non-small-cell lung cancer; TKI, tyrosine kinase inhibitor. Slide credit: clinicaloptions.com

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