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Metabo-Oncology
Cutting Off Cancer's Supply Chain

Cancer needs large amounts of glucose, fat and nutrients to grow and spread.  Dysregulated metabolic hormones associated with obesity, diabetes and metabolic syndrome help cancer gain access to these energy stores.
Metabo-oncology is the research behind understanding this symbiotic relationship – and disrupting it.

Why it matters

A Needed New Approach to Cancer Treatment

Cancer remains one of the toughest diseases to treat, and dysregulated metabolic hormones like insulin and leptin — often linked to obesity and diabetes — make it even harder.
SynDevRx’s lead compound, Evexomostat (SDX-7320), is a dual-action drug candidate being developed specifically to address this long-neglected unmet medical need.

Evexomostat is intended for cancer patients whose metabolic state may contribute to their disease progression and malignancy.

Baseline Metabolic Dysfunction

Overweight / Obesity

Pre-diabetes

Metabolic syndrome

Dyslipidemia

Type 2 diabetes

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Treatment-induced conditions

Hyperglycemia

Hyperinsulinemia

Pre-diabetes

Weight gain

Type 2 diabetes

Highly Vascularized Tumors

Many solid tumors are known to be highly vascularized, making them more aggressive:

Breast cancer

Prostate cancer

Renal cell carcinoma

Hepatocellular Carcinoma (HCC)

Thyroid Cancer

Glioblastoma

Soft tissue cancers (sarcomas)

and Metastatic tumors in general

Please see below for information on clinical trials in progress or planned for SDX-7320.

Treating Cancer and Metabolic Hormone Dysfunction It’s a fact: Overweight people or those with excess belly fat, type 2 diabetes or pre-diabetes, are more likely to get — and die from — cancer. In 14% of men and 20% of women (U.S.), deaths by cancer are directly related to dysregulated metabolic hormones. Insulin, leptin and adiponectin are among the most commonly dysregulated metabolic hormones. They can contribute to tumor growth and metastases (insulin, leptin) or suppress tumor growth (adiponectin). Addressing these metabolic hormones in cancer patients is critical for standard-of-care therapies to work to their full potential. SynDevRx is developing the first clinical drug candidate – evexomostat/SDX-7320 – specifically targeting this important unmet medical need. Esophageal Cancer Men with a body mass index (BMI) between 30 and 34.9 were found to have a 1.28-fold (i.e. 28%) increase in the relative risk of death from esophageal cancer while men with a body mass index (BMI) between 35 and 39.9 were found to have a 1.63-fold (i.e. 63%) increase in the relative risk of death from esophageal cancer (Calle et al, New Eng J Med; 2003, 348(17):1625-38). In this study there was no statistically significant increase in the relative risk of death from esophageal cancer in women with increased BMI. Increased risk of death from cancer when obese: Breast Cancer Post-menopausal women with a body mass index (BMI) between 30 and 34.9 were found to have a 1.6-fold (i.e. 60%) increase in the relative risk of death from breast cancer (Calle et al, 2003, New Eng J Med, 348(17):1625-38). In the same study, women with a body mass index (BMI) between 35 and 39.9 were found to have a 1.7-fold (i.e. 70%) increase in the relative risk of death from breast cancer, and women with a BMI ≥ 40 had a 2.1-fold (i.e. 112%) increase in the relative risk of death from breast cancer. Increased risk of death from cancer when obese: Liver Cancer Men with a body mass index (BMI) between 35 and 39.9 were found to have a 4.52-fold (i.e. 352%) increase in the relative risk of death from liver cancer (Calle et al, 2003, New Eng J Med, 348(17):1625-38). In the same study, women with a body mass index (BMI) between 35 and 39.9 were found to have a 1.68-fold (i.e. 68%) increase in the relative risk of death from liver cancer. Increased risk of death from cancer when obese: Pancreatic Cancer Men with a body mass index (BMI) between 35 and 39.9 were found to have a 1.49-fold (i.e. 49%) increase in the relative risk of death from pancreatic cancer (Calle et al, 2003, New Eng J Med, 348(17):1625-38). In the same study, women with a body mass index (BMI) between 35 and 39.9 were found to have a 1.41-fold (i.e. 41%) increase in the relative risk of death from pancreatic cancer, while women with a BMI ≥ 40 had a 2.76-fold (i.e. 176%) increase in the relative risk of death from pancreatic cancer. Increased risk of death from cancer when obese: Uterine (endometrial) Cancer Women with a body mass index (BMI) between 30 and 34.9 were found to have a 2.53-fold (i.e. 153%) increase in the relative risk of death from uterine/endometrial cancer (Calle et al, New Eng J Med; 2003, 348(17):1625-38). In the same study, women with a body mass index (BMI) between 35 and 39.9 were found to have a 2.77-fold (i.e. 177%) increase in the relative risk of death from uterine/endometrial cancer, while women with a BMI ≥ 40 had a 6.25-fold (i.e. 525%) increase in the relative risk of death from uterine/endometrial cancer. Increased risk of death from cancer when obese: Ovarian Cancer Women with a body mass index (BMI) between 30 and 34.9 were found to have a 1.16-fold (i.e. 16%) increase in the relative risk of death from ovarian cancer (Calle et al, New Eng J Med; 2003, 348(17):1625-38). In the same study, women with a body mass index (BMI) between 35 and 39.9 were found to have a 1.51-fold (i.e. 51%) increase in the relative risk of death from ovarian cancer. A more recent meta-analysis of nine studies found that women who were obese (BMI ≥ 30) had a 1.17-fold (i.e. 17%) increase in risk of dying from ovarian cancer (Nagle et al, British J Cancer, 2015; 113:817–26. Increased risk of death from cancer when obese: Colorectal Cancer Men with a body mass index (BMI) between 35 and 39.9 were found to have a 1.84-fold (i.e. 84%) increase in the relative risk of death from colorectal cancer while women with a body mass index (BMI) between ≥ 40 were found to have a 1.46-fold (i.e. 46%) increase in the relative risk of death from colorectal cancer (Calle et al, New Eng J Med; 2003, 348(17):1625-38). Increased risk of death from cancer when obese:

Drug Conjugation

Conjugating, or attaching, small molecules to a polymer backbone, is a clinically validated approach to improving small molecule drug safety and activity.

Optimizing Drug Conjugates

SDX has developed core expertise in improving the safety and efficacy of active small molecules via our deep understanding of polymer-drug conjugation chemistry and manufacturing.
The intrinsic properties of our polymer-drug conjugate change the bio-distribution and pharmacokinetic profile of the active small molecule, making it safer and more effective.

Anti-Angiogenesis, A validated anti-tumor treatment Modality

Cancer demands increasing amounts of oxygen and nutrients to proliferate and metastasize. To achieve this, cancer cells send out signals to the blood vessels, stimulating new blood vessel growth in a complex series of steps called angiogenesis. 

Anti-angiogenesis is the treatment modality used to limit a tumor’s access to blood. Our lead drug candidate evexomostat and drugs from the MetAP2 inhibitor class achieve their anti-angiogenic effects by inhibiting endothelial cell proliferation. 

  • What It Is – cutting off the tumor’s access to blood, oxygen and nutrients

  • Importance – restricting a tumor’s access to blood vessels ‘starves’ the tumor, making combination treatments more effective.

  • Cancer Indications – Cancers that are highly vascularized and rely on angiogenesis to grow and spread include:

    • Breast (TNBC, HR+)
    • Prostate
    • Glioblastoma
    • Renal (clear-cell)
    • Hepatocellular
    • Thyroid
    • Angiosarcoma

 

Evexomostat is a potent anti-angiogenic drug candidate being developed for use in combination with standard-of-care treatments for metabolically-sensitive cancers.

Scientific Presentations

SABCS-2024
Amelia-1: Evexomostat Clinical Trials in Progress

AACR-2023
Evexomostat (SDX-7320) Shows Potent Anti-Tumor, Anti-Angiogenic Activity in Multiple Models of Prostate Cancer

SABCS-2022
Evexomostat (SDX-7320) Prepares Amelia-1 Study in Combination with PI3K Inhibitor Plus Fulvestrant

AICR-2022
SDX-7320 Demonstrates Both Anti-Tumor and Anti-Diabetic Activity in Multiple Animal Models

SABCS-2021
SDX-7320 Enhances AKT Inhibitor Activity via Suppression of Hypoxia- and Inflammatory-Related Genes

AACR-2020
SDX-7320 Phase 1 Safety Study Results: Improvements in Angiogenic and Metabolic Markers

SABCS-2019
SDX-7320 Shows Anti-Tumor Synergy and Improves Glucose Control with PI3K Inhibitor

AACR-2019
SDX-7320 Improves Tumor Immune Micro-Environment in TNBC Model (EO771)

AACR-2018
SDX-7320 Enhanced Activity in Models of Obesity-Driven Cancer (EO771 TNBC, B16F10 Melanoma)

AACR-2023
Evexomostat (SDX-7320) Shows Potent Anti-Tumor, Anti-Angiogenic Activity in Multiple Models of Prostate Cancer

AACR-2023
Evexomostat (SDX-7320) Shows Potent Anti-Tumor, Anti-Angiogenic Activity in Multiple Models of Prostate Cancer

SABCS-2022
Evexomostat (SDX-7320) Prepares Amelia-1 Study in Combination with PI3K Inhibitor Plus Fulvestrant

AICR-2022
SDX-7320 Demonstrates Both Anti-Tumor and Anti-Diabetic Activity in Multiple Animal Models

SABCS-2021
SDX-7320 Enhances AKT Inhibitor Activity via Suppression of Hypoxia- and Inflammatory-Related Genes

AACR-2020
SDX-7320 Phase 1 Safety Study Results: Improvements in Angiogenic and Metabolic Markers

SABCS-2019
SDX-7320 Shows Anti-Tumor Synergy and Improves Glucose Control with PI3K Inhibitor

AACR-2019
SDX-7320 Improves Tumor Immune Micro-Environment in TNBC Model (EO771)

AACR-2018
SDX-7320 Enhanced Activity in Models of Obesity-Driven Cancer (EO771 TNBC, B16F10 Melanoma)

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