CAMP4 gets Australian clearance to start CMP-002 trial in SYNGAP1 disorder

CAMP4 Therapeutics Corporation said on July 27, 2026 that it had received clearance from Australia's Therapeutic Goods Administration and local Human Research Ethics Committee to initiate its Phase 1/2 clinical trial of CMP-002, a potential first-in-class disease-modifying therapeutic for SYNGAP1-related disorder.¹

The clearance carries financial consequences beyond the trial itself. CAMP4 said the clearance meant the company achieved the CTA Milestone defined under its September 9, 2025 Securities Purchase Agreement, and it also received a Price Threshold Waiver under that agreement, which together satisfied the Second Closing Trigger.¹ As a result, CAMP4 is eligible to receive up to approximately $50.1 million in gross proceeds from the Second Closing, in exchange for up to 32,721,172 shares of common stock, or for certain investors, pre-funded warrants in lieu of common stock.¹ The Second Closing is expected to occur on or about August 3, 2026, subject to customary closing conditions.¹

Investors committed to the second tranche include Coastlands Capital, Janus Henderson Investors, Balyasny Asset Management, Vivo Capital, 5AM Ventures, Adage Capital Management LP, Trails Edge Capital Partners, and CURE SYNGAP1, according to the release. Leerink Partners is serving as lead placement agent, with Piper Sandler & Co., Cantor Fitzgerald & Co. and Wedbush Securities Inc. acting as co-placement agents.¹

On the clinical side, the Australian clearance allows CAMP4 to open a trial site there, expected to be one of the initial enrollment sites for the Phase 1/2 study, with Australia chosen as the first regulatory filing jurisdiction due to regional expertise in SYNGAP1 diagnosis and treatment and the TGA's review process.¹ CAMP4 said it continues to pursue regulatory filings in other jurisdictions to support broader enrollment.¹

CMP-002 is an antisense oligonucleotide candidate. It is designed to bind to a SYNGAP1-specific regulatory RNA to increase SYNGAP1 gene expression and restore SYNGAP protein toward near wild-type levels.¹ There are currently no approved disease-modifying therapies for SYNGAP1-related disorder.¹