ALX Oncology Presents New Data from Fully Enrolled ALX148 Clinical Trial Combination Cohorts for the Treatment of Patients with Advanced Solid Tumors

New Clinical Data Presented at the 2019 American Society of Clinical
Oncology (ASCO) in Chicago, IL

DUBLIN & BURLINGAME, Calif.–(BUSINESS WIRE)–ALX Oncology, a clinical-stage immuno-oncology company developing
therapies to block the CD47 myeloid checkpoint mechanism, today
announced new results from its Phase 1 ALX148 solid tumor program at the
2019 ASCO Annual Meeting [Abstract
]. As of April 18, 2019, eighty-two patients with various
advanced malignancies were administered ALX148 in combination with
standard regimens of either trastuzumab (n=30) or pembrolizumab (n=52).
Objective responses were observed in expansion cohorts for both
gastric/gastroesophageal junction cancer (G/GEJ) and squamous cell
carcinoma of the head and neck (HNSCC). Key results are:

  • In response-evaluable patients with HER2 positive G/GEJ (n=18) whose
    tumors had failed prior HER2-targeted therapy, an overall response
    rate (ORR) of 22% and a disease control rate (DCR) of 28% were
  • In patients with HNSCC (n=19) whose tumors had failed prior platinum
    therapy, an ORR of 16% and a DCR of 26% were observed. In checkpoint
    naïve subjects (n=10), an ORR of 30% and a DCR of 30% were observed.
  • ALX148 was well tolerated and the most common treatment-related
    adverse event in combination with trastuzumab was grade 1/2 fatigue
    (27%), and with pembrolizumab was grade 1/2 increased AST (15%).
  • Preliminary data from paired pre- and on-study tumor biopsies from
    combination cohorts showed a statistically significant increase in
    intra-tumoral macrophages following ALX148 treatment, consistent with
    ALX148’s mechanism of action as a myeloid checkpoint inhibitor.

“Emerging anti-tumor activity of ALX148 combined with anti-cancer
antibodies supports our hypothesis that blocking CD47 with an
Fc-inactive molecule can enhance the anti-cancer immune response in
patients with varying solid tumor malignancies,” said Sophia Randolph
M.D., Ph.D., Chief Medical Officer of ALX Oncology. “With its clinical
activity and consistent safety profile, ALX148 may become a new
cornerstone of immune therapy. We are excited to continue evaluating its
clinical benefit in populations in need of novel treatments.”

About ALX148
ALX148, designed for combination therapy, is a
fusion protein comprised of an engineered high affinity CD47 binding
domain of SIRPα linked to an inactive Fc region of human immunoglobulin.
ALX148 potently and specifically binds CD47 and blocks its interaction
with SIRPα, thus inhibiting a key immune checkpoint mechanism exploited
by cancer cells. In preclinical studies, ALX148 bridges innate and
adaptive immunity to maximize anti-tumor response in combinations with
targeted anti-cancer antibodies and checkpoint inhibitors via
Fc-dependent and Fc-independent mechanisms. No adverse effects on
CD47-expressing normal blood cells were seen in ALX148 preclinical

The ALX148 Phase 1 clinical trial is a two-part study that evaluates the
safety, pharmacokinetics, and pharmacodynamics of ALX148. Enrollment to
the combination therapy portion in which ALX148 is administered with
approved anti-cancer antibodies is ongoing. For more information about
the Phase 1 study, please visit clinicaltrials.gov,
identifier number NCT03013218.

About ALX Oncology
ALX Oncology is a clinical-stage
immuno-oncology company developing therapies that block the CD47
checkpoint mechanism, which is exploited by cancer cells to evade the
immune system. Our lead candidate, ALX148, is a fusion protein comprised
of an engineered high affinity CD47 binding domain of SIRPα linked to an
inactive Fc region of human immunoglobulin. ALX148 is designed to
maximize the clinical benefit of antibody-based therapies and is in
clinical development for a broad range of tumor types. www.alxoncology.com


Karen Sharma
(781) 235-3060
[email protected]

Read the full article

Leave a Reply

Your email address will not be published. Required fields are marked *

This site uses Akismet to reduce spam. Learn how your comment data is processed.