Pipeline - Alterome

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

AKT1 E17K (ALTA2618)

Phase 1/1B

Breast and endometrial cancers, solid tumors

KRAS selective (ALTA3263)

Phase 1/1B

CRC, PDAC, NSCLC, solid tumors

Undisclosed

Discovery

Solid tumors

Discovery

Solid tumors

ALTA2618: Ushering in the precision era for AKT-targeted therapies

ALTA2618 is a clinical-stage, first-in-class, mutation-specific inhibitor of AKT1 E17K, a key driver mutation present in up to 90% of AKT-activated cancers. Engineered for selectivity, potency, and a broad therapeutic index, ALTA2618 is designed to overcome the safety and efficacy limitations of pan-AKT inhibitors. By targeting the mutant protein while sparing wild-type AKT isoforms, indication-agnostic ALTA2618 is intended to deliver more durable and tolerable responses across a range of solid tumors.

Learn about
AKT-driven
cancers

ALTA2618 targets the disease-driving AKT1 E17K mutation while sparing wild-type AKT

Covalent binding to AKT1 and mutant selectivity could potentially allow for lower efficacious doses and a more favorable tolerability profile.

ALTA2618 incorporates multiple layers of precision engineering to potentially overcome the safety and efficacy limitations of earlier AKT inhibitors:

AKT1 isoform specificity – Designed to eliminate AKT2-driven toxicities (e.g. hyperglycemia)
Allosteric inhibition – May reduce the need to compete with ATP at the kinase active site, potentially lowering the efficacious dose
AKT1 E17K mutation specificity intended to spare wild-type AKT1 – May mitigate on-target toxicity and improve tolerability; may also improve the therapeutic index and reduce systemic side effects based on preclinical models
Covalent capture of the mutant lysine (E17K) – Designed to lock AKT1 in a closed, inactive conformation to suppress oncogenic signaling
Enhanced target coverage – Shown preclinically to drive stronger, more durable responses, which may translate to higher overall response rates across solid tumor types

NOW ENROLLING

AKTive-001 clinical trial

This Phase 1/1b clinical trial, looking at the safety and tolerability of ALTA2618, is enrolling adults with advanced solid tumors with an AKT1 E17K mutation.

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

The promise of pan-KRAS and ALTA3263

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

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 <1nM potency across >90% of KRAS mutations, including common drivers (e.g., G12D, G12V) and resistance-associated variants. Targets WT KRAS to shut down compensatory signaling and help prevent 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 excellent 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 without compromising safety, 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 clinical trial

We are currently enrolling people with advanced solid tumors with KRAS mutations into a Phase 1 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

ALTA2618: Ushering in the precision era for AKT-targeted therapies

ALTA2618 targets the disease-driving AKT1 E17K mutation while sparing wild-type AKT

ALTA2618 incorporates multiple layers of precision engineering to potentially overcome the safety and efficacy limitations of earlier AKT inhibitors:

NOW ENROLLING

AKTive-001 clinical trial

The promise of pan-KRAS and ALTA3263

ALTA3263 offers:

ALTA3263 inhibits both ON and OFF states

NOW ENROLLING

Phase 1 clinical trial

Contact us

Advancing

medicines designed to change the treatment paradigm

Developing alteration-specific therapies that cancers can’t evade

ALTA2618: Ushering in the precision era for AKT-targeted therapies

ALTA2618 targets the disease-driving AKT1 E17K mutation while sparing wild-type AKT

ALTA2618 incorporates multiple layers of precision engineering to potentially overcome the safety and efficacy limitations of earlier AKT inhibitors:

NOW ENROLLING

AKTive-001 clinical trial

The promise of pan-KRAS and ALTA3263

ALTA3263 offers:

ALTA3263 inhibits both ON and OFF states

NOW ENROLLING

Phase 1 clinical trial

Contact us

medicines designed to change
the treatment paradigm