# Sustained Complete Response to Brigatinib in a Young Patient With ALK‐Positive NSCLC Harboring I1171N Mutation Post‐Alectinib Resistance

**Authors:** Akhil Kapoor, Ajay Kumar Singh, Mahesh Chaudhary, Anuj Gupta, Bipinesh Sansar, Bal Krishna Mishra, Shashikant Patne, Arvind Suresh

PMC · DOI: 10.1155/crom/7372418 · Case Reports in Oncological Medicine · 2026-02-19

## TL;DR

A young patient with ALK-positive lung cancer achieved long-term remission with brigatinib after developing resistance to alectinib.

## Contribution

Demonstrates brigatinib's effectiveness against I1171N mutation in ALK-positive NSCLC after alectinib resistance.

## Key findings

- Brigatinib induced a complete and sustained response in a patient with I1171N-mediated alectinib resistance.
- Durable intracranial disease control was observed with brigatinib treatment.
- Repeat molecular testing was critical in identifying the resistance mutation and guiding treatment.

## Abstract

ALK‐rearranged non–small cell lung cancer (NSCLC) represents a paradigm of precision oncology, but acquired resistance to second‐generation ALK tyrosine kinase inhibitors (TKIs) such as alectinib remains inevitable. We report a young, nonsmoker male with ALK‐positive metastatic NSCLC who achieved a sustained complete response (CR) to brigatinib following alectinib resistance mediated by the ALK I1171N mutation. After 22 months of response to alectinib, disease progression prompted repeat molecular profiling, which identified the I1171N alteration. Brigatinib was initiated, and a complete radiologic response was documented within 3 months and has been sustained for over 12 months, including durable intracranial disease control. Sustained CR in I1171N‐mediated alectinib resistance is rare and highlights the critical role of repeat molecular testing to guide ALK TKI sequencing.

## Linked entities

- **Genes:** ALK (ALK receptor tyrosine kinase) [NCBI Gene 238]
- **Chemicals:** Brigatinib (PubChem CID 68165256), Alectinib (PubChem CID 49806720)
- **Diseases:** Non–small cell lung cancer (MONDO:0005233)

## Full-text entities

- **Genes:** EML4 (EMAP like 4) [NCBI Gene 27436] {aka C2orf2, ELP120, EMAP-4, EMAPL4, ROPP120}, ABCG2 (ATP binding cassette subfamily G member 2 (JR blood group)) [NCBI Gene 9429] {aka ABC15, ABCP, BCRP, BMDP, CD338, CDw338}, TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}, EGFR (epidermal growth factor receptor) [NCBI Gene 1956] {aka ERBB, ERBB1, ERRP, HER1, NISBD2, NNCIS}, ALK (ALK receptor tyrosine kinase) [NCBI Gene 238] {aka ALK1, CD246, NBLST3}, ROS1 (ROS proto-oncogene 1, receptor tyrosine kinase) [NCBI Gene 6098] {aka MCF3, ROS, c-ros-1}
- **Diseases:** metabolic toxicities (MESH:D065606), lymphadenopathy (MESH:D008206), NSCLC (MESH:D002289), dyslipidemia (MESH:D050171), CPK (OMIM:123320), alterations (MESH:D004408), cerebral metastasis (MESH:D009362), liver, nodal, and osseous lesions (MESH:D008107), intracranial disease (MESH:D020765), toxicity (MESH:D064420), cough (MESH:D003371), cancer (MESH:D009369), adenocarcinoma (MESH:D000230), lung mass (MESH:D008171), bony lesions (MESH:D000070896)
- **Chemicals:** atezolizumab (MESH:C000594389), Alectinib (MESH:C582670), bevacizumab (MESH:D000068258), lead (MESH:D007854), carboplatin (MESH:D016190), lorlatinib (MESH:C000590786), Brigatinib (MESH:C000598580), FDG (MESH:D019788), paclitaxel (MESH:D017239)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** L1196M, D1203N, G1269A, C1156Y, G1202R, S1206Y, V1180L, L1256F, L1198F, I1171N, F1174C

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12920669/full.md

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12920669/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920669/full.md

---
Source: https://tomesphere.com/paper/PMC12920669