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‘γδT세포 타깃’ 임첵, 시리즈B 600만弗 추가 유치 - 바이오스펙테이터

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‘γδT세포 타깃’ 임첵, 시리즈B 600만弗 추가 유치

입력 2020-09-16 15:26 수정 2020-09-16 15:26

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600만달러 시리즈B 추가 투자 총 5400만달러 투자 유치...감마델타T세포 타깃 단일항체 임상개발에 사용...현재 고형암, 혈액암 대상 임상1상 진행 중

감마델타(γδ, Gammadelta)T세포를 활성화하는 단일항체를 개발하는 임첵(ImCheck)이 시리즈B에 600만달러를 추가로 투자받았다. 작년 12월 시리즈B 투자를 마감한지 9개월 만이다.

임첵은 시리즈B로 600만달러를 추가 투자받아 총 5400만달러의 투자금을 유치했다고 지난 15일(현지시간) 밝혔다. 여기에 퓨레오스(Pureos), 비피프랑스(Bpifrance), 화이자벤쳐스(Pfizer Ventures), 웰링턴파트너스(Wellington Partners), 에이전트캐피탈(Agent Capital), 알렉산드리아벤처인베스트먼츠(Alexandria Venture Investments)가 새롭게 참여했다. 기존 시리즈A 투자자인 베링거인겔하임벤처(Boehringer Ingelheim Venture), 컬마파트너스(Kurma Partners), 아이딘베스트파트너스(Idinvest Partners), 라이프사이언스파트너스(Life Sciences Partners), 김브(Gimv)도 이번 시리즈B에 참여했다.

이번 투자금은 γδT세포의 항암면역 반응을 활성화시키는 부티로필린(Butyrophilin) 작용제(Agonist) ‘ICT01’의 임상1/2a상을 위해 쓰일 예정이다. 부티로필린은 면역세포와 암세포 모두에서 발현하는 면역 조절 단백질이다.

지금까지 CAR-T 치료제는 알파베타(αβ, Alphabeta) T세포를 기반으로 개발됐다. 알파베타T세포의 T세포 수용체는 α-사슬(Chain)과 β-사슬로 구성되어 있다. T세포 수용체가 항원제시세포(Antigen Presenting Cell)의 주조직적합성복합체(MHC)에 의해 제시되는 암 항원을 인지해 항암면역반응을 일으킨다. 암 종마다 다르지만 약 15~96%까지 MHC의 발현을 억제해 항암 면역반응을 회피한다.

이를 극복하고자 최근 감마델타 T세포가 주목받고 있다. 감마델타T세포의 T세포 수용체는 γ-사슬과 δ-사슬로 구성되어 있고 전체 T세포의 약 2~3%를 차지한다. 특이한 점은 MHC에 의존하지 않고 암세포를 죽일 수 있다. 암세포처럼 비정상적인 대사작용을 하는 세포에서 축적되는 비펩타이드 인 항원(Non-Peptide Phosphoantigen)을 인식하여 항암면역 반응을 일으킨다. 아직까지 메커니즘은 정확히 밝혀지지 않았다.

임첵은 암세포에서 발현하는 면역조절인자 BTN3A가 감마델타T세포 활성에 중요하다고 설명했다. 암세포 내에서 생성된 비펩타이드 인 항원이 BTN3A의 세포 내 도메인과 결합한다. 이 결합이 BTN3A의 세포 밖 도메인의 형태 변화를 유도해 감마델타T세포의 항암면역반응을 활성화한다. BTN3A 작용제 ICT01은 BTN3A의 형태 변화를 유도해 감마델타T세포에 의한 암세포 사멸을 촉진하는 메커니즘이라고 회사측은 설명했다.

임첵은 올해 2월 고형암, 혈액암 환자를 대상으로 ICT01의 임상1상을 시작했으며 2022년말 종료할 예정이다(EVICTION, NCT04243499).

▲*ICT01의 작용 메커니즘(임첵 웹사이트)

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