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SYNTHIS THERAPEUTICS, INC.

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Company Details

Name: SYNTHIS THERAPEUTICS, INC.
Jurisdiction: New York
Legal type: FOREIGN BUSINESS CORPORATION
Status: Active
Date of registration: 21 Sep 2020 (5 years ago)
Entity Number: 5839855
ZIP code: 10016
County: New York
Place of Formation: Delaware
Address: 430 EAST 29TH STREET, ALEXANDRIA LAUNCHLABS, 14TH FL, NEW YORK, NY, United States, 10016

DOS Process Agent

Name Role Address
THE CORPORATION DOS Process Agent 430 EAST 29TH STREET, ALEXANDRIA LAUNCHLABS, 14TH FL, NEW YORK, NY, United States, 10016

Commercial and government entity program

CAGE number:
7NWT8
Status:
Obsolete
Type:
Non-Manufacturer
CAGE Update Date:
2025-02-04
SAM Expiration:
2026-01-31

Contact Information

POC:
DORI A. KARYAT

Filings

Filing Number Date Filed Type Effective Date
200921000283 2020-09-21 APPLICATION OF AUTHORITY 2020-09-21

USAspending Awards / Financial Assistance

Date:
2024-09-18
Awarding Agency Name:
Department of Health and Human Services
Transaction Description:
IN VIVO EFFICACY, SAFETY AND PK/PD ANALYSIS OF SYN101, A FIRST IN CLASS, IMMUNE CELL TARGETED TGFB THERAPY FOR CANCER PATIENTS - NCI SBIR PHASE II SUMMARY THE IMMUNE CHECKPOINT INHIBITORS (ICI) BLOCK A SINGLE IMMUNO-SUPPRESSIVE PATHWAY IN CANCER PATIENTS. HOWEVER, ACROSS ALL CANCERS, LESS THAN 30% OF PATIENTS RESPOND TO ICI THERAPIES, DUE TO ADDITIONAL BRAKES ON THE IMMUNE SYSTEM, WHICH LIMIT EFFICACY. THE IMMUNO-SUPPRESSIVE CYTOKINE, TGF− IS ONE OF THOSE “BRAKES” THAT DRIVES CHECKPOINT RESISTANCE IN MULTIPLE SOLID TUMORS SUCH AS COLORECTAL, BLADDER, PROSTATE, HEAD AND NECK CANCERS AND MELANOMA. LEVELS OF TGF− INCREASE AS THE CANCER BECOMES MORE AGGRESSIVE, DRIVING A WORSE PATIENT PROGNOSIS. IN ADDITION TO MAINTAINING TISSUE HEALTH AND HOMEOSTASIS, TGF− IS A VALIDATED TUMOR PROMOTING CYTOKINE WITH HAS MULTIPLE ROLES IN CANCER DEVELOPMENT, INCLUDING IMMUNE SUPPRESSION, INCREASING ANGIOGENESIS AND DRIVING METASTASIS. DESPITE LONG STANDING INTEREST IN TGF− BLOCKADE AS A CANCER THERAPY, CLINICAL DEVELOPMENT HAS BEEN HAMPERED FOR TWO MAIN REASONS: 1) SIGNIFICANT HOST (I.E., CARDIAC) TOXICITY AND 2) THE POTENTIAL TO CONVERT INDOLENT EARLY STAGE TUMORS INTO MORE AGGRESSIVE ONES. HOWEVER, IN PRECLINICAL STUDIES, BLOCKADE OF THE TGF− PATHWAY ONLY IN T CELLS IS SUFFICIENT FOR TUMOR CLEARANCE IN VIVO. THUS, A THERAPY THAT ELIMINATES TGF− SIGNALING SOLELY IN IMMUNE CELLS WOULD DRIVE TUMOR CLEARANCE, WHILE AVOIDING THE ADVERSE EVENTS DEMONSTRATED BY SYSTEMIC TGF− THERAPIES. WITH BOTH A PHASE I SBIR GRANT AND VENTURE FUNDING, WE HAVE GENERATED SYN101, A PROPRIETARY IMMUNE CELL TARGETED TGF- THERAPEUTIC (SYN101) THAT SELECTIVELY REVERSES TGF- MEDIATED IMMUNE SUPPRESSION, WHILE SPARING HOST TISSUE TOXICITY. WE HAVE DEMONSTRATED THAT MONOTHERAPY SYN101 DRIVES TUMOR CLEARANCE AND SURVIVAL IN SYNGENEIC MOUSE TUMOR MODELS, WITH CORRESPONDING IMMUNE CELL ACTIVATION MARKERS IN THE BLOOD AND TUMOR MICROENVIRONMENT. MOREOVER, SYN101 DOES NOT CAUSE CARDIAC TOXICITY AT EFFICACIOUS DOSES IN VIVO. IN THIS PHASE II SBIR APPLICATION, WE WILL PERFORM ADDITIONAL IN VIVO EFFICACY, SAFETY AND PK STUDIES WITH OUR SYN101 DEVELOPMENT CANDIDATE, WHICH WILL LEAD TO IND ENABLING STUDIES. IN AIM 1, WE WILL TEST EFFICACY OF HUMAN SYN101 IN HUMANIZED MOUSE TUMOR MODELS, ALONG WITH CORRESPONDING LYMPHOCYTE PD MARKERS IN THE BLOOD AND TUMOR MICROENVIRONMENT. USING CYTOF ANALYSIS, WE WILL DEFINE THE COMPREHENSIVE IMMUNE RESPONSE DRIVEN BY SN101 IN VIVO, AS A STEP TOWARDS IDENTIFYING BIOMARKERS OF TGF- TARGET ENGAGEMENT IN CLINICAL TRIALS. IN AIM 2, WE WILL TEST THE SAFETY AND TOXICITY OF SYN101 IN SPRAGUE DAWLEY RATS, THE INDUSTRY STANDARD FOR SYSTEMIC TGF- INHIBITOR TOXICITY. IN ADDITION, WE WILL PERFORM PK STUDIES, TO ROUND OUT THE FULL PRECLINICAL DATA PACKAGE. WHILE WE DO NOT ANTICIPATE SIGNIFICANT TOXICITY FROM SYN101, THESE STUDIES WILL DERISK THE PLATFORM, ESTABLISH EFFICACY AND SAFETY, AND SUPPORT ENTRY INTO IND ENABLING. VIRTUALLY EVERY ADVANCED TUMOR HAS ELEVATED TGF− LEVELS, SUCH THAT A SAFER, MORE EFFICACIOUS TARGETED TGF- THERAPY WOULD BE BENEFICIAL FOR A SIGNIFICANT PORTION OF CANCER PATIENTS. SYN101 WILL PROVIDE NEW THERAPEUTIC OPTIONS FOR REFRACTORY CANCER PATIENTS AND WILL SAFELY REVERSE IMMUNE SUPPRESSION TO IMPROVE PATIENT RESPONSE RATES.
Obligated Amount:
578977.00
Face Value Of Loan:
0.00
Total Face Value Of Loan:
0.00
Date:
2023-05-08
Awarding Agency Name:
Department of Health and Human Services
Transaction Description:
DEVELOPMENT OF A TARGETED TGF-B THERAPEUTIC THAT SELECTIVELY BLOCKS LUNG FIBROSIS IN IDIOPATHIC PULMONARY FIBROSIS (IPF) PATIENTS - SYNTHIS PROJECT SUMMARY/ABSTRACT PHASE I NHLBI IPF IS A CHRONIC, IRREVERSIBLE FIBROTIC LUNG DISEASE DRIVEN BY REPEATED INJURY, RESULTING IN PROGRESSIVE STIFFENING AND ULTIMATELY, LOSS OF LUNG FUNCTION. WITH 130,000 IPF PATIENTS ANNUALLY AND A 5 YEAR MORTALITY RATE OF 80%, THERE IS SIGNIFICANT NEED FOR NEW THERAPIES. TO DATE, CONVENTIONAL THERAPIES HAVE NOT HALTED DISEASE PROGRESSION. RECENTLY 2 NEW IPF DRUGS WERE APPROVED: PIRFENIDONE, AN ANTI-FIBROTIC AGENT AND, NINTEDANIB, A TYROSINE KINASE INHIBITOR, BUT BOTH ONLY MODESTLY DELAY DISEASE PROGRESSION. TGF- IS ONE OF THE KEY DRIVERS OF FIBROSIS IN IPF PATIENTS, DUE TO ITS ELEVATED AND PROLONGED LEVELS IN THE LUNG. ON A CELLULAR LEVEL, TGF- DRIVES ACTIVATED MYOFIBROBLASTS, THE MAJOR PERPETRATORS OF DISEASE, TO OVER-PRODUCE COLLAGEN AND INCREASE FIBRONECTIN DEPOSITION IN THE EXTRACELLULAR MATRIX (ECM), WHICH PROGRESSIVELY BLOCKS LUNG FUNCTION. INHIBITION OF TGF-- MEDIATED FIBROSIS COULD POTENTIALLY STOP OR EVEN REVERSE DISEASE IN IPF PATIENTS. HOWEVER, TGF- IS WIDELY EXPRESSED AND HAS ESSENTIAL ROLES IN MAINTAINING TISSUE HOMEOSTASIS. THUS, ALTHOUGH TGF- INHIBITORS ARE OF SIGNIFICANT INTEREST TO TREAT FIBROSIS, DEVELOPMENT OF THERAPIES HAS BEEN HINDERED DUE TO SIGNIFICANT HOST (I.E., CARDIAC) TOXICITY. SAFER TGF- INHIBITORS THAT SELECTIVELY BLOCK FIBROSIS IN IPF PATIENTS, BUT STILL PROTECT HOST TISSUES, WOULD PROVIDE DIFFERENTIATED TREATMENT OPTIONS TO FILL THIS SIGNIFICANT UNMET NEED. IN THIS SBIR AWARD, WE ARE DEVELOPING A FIRST IN CLASS ANTIBODY DRUG CONJUGATE (ADC) PLATFORM TO SELECTIVELY INHIBIT TGF- DRIVEN FIBROSIS IN IPF PATIENTS. IN AIM 1, WE WILL DEVELOP OUR NOVEL ADC THERAPEUTIC (SYN301) AND DEMONSTRATE INHIBITION OF FIBROSIS IN FIBROBLASTS DERIVED FROM IPF PATIENTS, AS ASSESSED BY A DECREASE IN PROCOLLAGEN EXPRESSION AND ALPHA SMOOTH MUSCLE ACTIN IN VITRO, CLINICAL MARKERS OF FIBROTIC DISEASE. IN AIM 2, WE WILL ASSESS THE EFFICACY OF SYN301 IN AN INDUSTRY STANDARD, IN VIVO MODEL OF BLEOMYCIN INDUCED LUNG FIBROSIS. SYN301 WILL BE ASSESSED FOR INHIBITION OF DISEASE PROGRESSION AND LUNG FIBROSIS AS MEASURED BY LUNG HISTOPATHOLOGY, INFLAMMATORY INFILTRATES, COLLAGEN DEPOSITION AND BALF IMMUNE CELL COMPOSITION. WE ANTICIPATE THAT SYN301 WILL REDUCE MARKERS OF FIBROSIS BOTH IN VITRO AND IN VIVO, COMPARED TO STANDARD OF CARE THERAPIES. SYN301 IS A FIRST IN CLASS THERAPY THAT WILL SAFELY BLOCK TGF- INDUCED FIBROSIS IN IPF PATIENTS. IT IS THE FIRST ADC MOLECULE BEING DEVELOPED TO SELECTIVELY BLOCK TGF- DRIVEN FIBROSIS. MOREOVER, SYN301 COULD ALSO BE USED IN COMBINATION WITH CURRENT FIBROSIS THERAPIES, TO INCREASE OVERALL PATIENT RESPONSE RATES. TISSUE FIBROSIS IS A WIDE SPREAD ISSUE IN MULTIPLE OTHER DISEASES, SUCH AS NASH, KIDNEY FIBROSIS AND CARDIAC FIBROSIS, OF WHICH TGF- IS ALSO INSTRUMENTAL IN DRIVING DISEASE. THUS, OUR THERAPEUTIC PLATFORM IS WIDELY APPLICABLE TO FIBROSIS IN MULTIPLE DISEASES, PROVIDING NOVEL THERAPEUTIC OPTIONS FOR PATIENTS THAT NEED IT THE MOST.
Obligated Amount:
299900.00
Face Value Of Loan:
0.00
Total Face Value Of Loan:
0.00
Date:
2019-07-31
Awarding Agency Name:
Department of Health and Human Services
Transaction Description:
DEVELOPMENT OF A NOVEL CHECKPOINT INHIBITOR-TGF BETA COMBINATION THERAPY TO REVERSE IMMUNE SUPPRESSION AND INCREASE SURVIVAL RATES IN ADVANCED COLORECTAL CANCER PATIENTS
Obligated Amount:
509975.00
Face Value Of Loan:
0.00
Total Face Value Of Loan:
0.00
Date:
2018-09-19
Awarding Agency Name:
Department of Health and Human Services
Transaction Description:
DEVELOPMENT OF A T CELL-TARGETED TGF-B ANTAGONIST THAT REVERSES IMMUNE SUPPRESSION IN MELANOMA PATIENTS
Obligated Amount:
299946.00
Face Value Of Loan:
0.00
Total Face Value Of Loan:
0.00

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Date of last update: 22 Mar 2025

Sources: New York Secretary of State