Advancing

medicines designed to change
the treatment paradigm

Developing alteration-specific therapies that cancers can’t evade

We are advancing a pipeline of next-generation, small molecule targeted therapies across a range of cancers.

Target

Indication

Discovery

preclinical

IND Enabling

Phase 1/1B

KRAS selective ALTA3263

Phase 1/1B

CRC, PDAC, solid tumors

Undisclosed

Discovery

Solid tumors

Discovery

Solid tumors

The promise of pan-KRAS and ALTA3263

ALTA3263 is our therapeutic candidate designed for broad, durable, and tolerable inhibition of KRAS-driven cancers. Developed to address the limitations of mutation-specific and pan-RAS inhibitors, we believe ALTA3263 combines deep target coverage with a favorable therapeutic index.

We are investigating ALTA3263 in a Phase 1/1b clinical trial in advanced solid tumors, with a focus on colorectal (CRC) and pancreatic ductal adenocarcinoma (PDAC) cancers. Nearly 50% of colorectal cancers harbor KRAS mutations, yet approved KRAS-targeted therapies address only a small subset of these mutations, highlighting the opportunity for new combination approaches targeting a broader range of KRAS mutations. KRAS mutations are present in more than 90% of PDAC cases, a cancer with significant unmet need, highlighting the opportunity for new KRAS-targeted combination therapies in earlier lines of treatment, where improving outcomes could have a meaningful impact on patients.

Learn about
KRAS-driven
cancers

ALTA3263 offers:

KRAS isoform selectivity – Targets KRAS while sparing HRAS and NRAS, aiming to reduce off-target toxicities and support more tolerable, combinable treatment regimens
Broad KRAS mutant and wild-type (WT) coverage – Demonstrated predominantly sub-nanomolar potency across KRAS mutations representing >90% of KRAS mutations by frequency, including common drivers (e.g., G12D, G12V) and resistance-associated variants. Targets WT KRAS to inhibit compensatory signaling and help limit therapeutic escape
Dual ON/OFF-state inhibition – Engineered to bind KRAS in both active (ON) and inactive (OFF) states, enabling inhibition of mutations like G12D and G12V that favor the ON state and are historically difficult to drug
Drug-like properties and pharmacokinetics profile – Designed for good oral bioavailability and pharmacokinetics, with the potential to achieve full, sustained target coverage and support monotherapy or combination use
Tolerability and combinability – Intended to deliver meaningful clinical activity while supporting tolerability and compatibility, offering a promising therapeutic backbone for use in combination with standard-of-care or emerging targeted therapies

ALTA3263 inhibits both ON and OFF states

Most KRAS inhibitors do not potently bind the ON state (as seen in preclinical models), which limits their ability to inhibit mutations like G12D and G12V that stay in the ON state longer.

NOW ENROLLING

Phase 1/1b clinical trial

We are currently enrolling people with advanced solid tumors with KRAS mutations into a Phase 1/1b study evaluating the safety, tolerability, pharmacokinetics, and preliminary clinical activity of ALTA3263.

Learn more or find a trial site near you at clinicaltrials.gov or email clinical.trials@alterome.com

Advancing

medicines designed to change the treatment paradigm

Developing alteration-specific therapies that cancers can’t evade

The promise of pan-KRAS and ALTA3263

ALTA3263 offers:

ALTA3263 inhibits both ON and OFF states

NOW ENROLLING

Phase 1/1b clinical trial

Contact us

medicines designed to change
the treatment paradigm