Leadiant Biosciences

Pipeline & Clinical Trials

Carnitine

Diabetes Mellitus, Type I

N/A

Clinical Trials (1)

NCT00351234Carnitine Levels and Carnitine Supplementation in Type I Diabetes

N/A

ERCP and Confocal imaging

Biliary Stricture

N/A

Clinical Trials (1)

NCT00892632Confocal Endomicroscopy for Biliary Strictures -Phase I

N/A

Chenodeoxycholic Acid

Cerebrotendinous Xanthomatoses

N/A

Clinical Trials (1)

NCT05499026Safety and Efficacy of CDCA in CTX Chenodeoxycholic Acid (CDCA) in Patients Affected by Cerebrotendinous Xanthomatosis (CTX)

N/A

cysteamine hydrochloride

Cystinosis

N/A

Clinical Trials (1)

NCT00010426Randomized Study of New Formulation Ophthalmic Cysteamine Hydrochloride for Corneal Cystine Accumulation in Patients With Cystinosis

N/A

PEG-L-asparaginase

T-Cell Lymphoma

PHASE_1

Clinical Trials (1)

NCT01878708A Pilot Study of Oncaspar® + Dexamethasone in Patients With Relapsed or Refractory T-Cell Lymphoma

Phase 1

STP206 or vehicle control

Healthy

PHASE_1

Clinical Trials (1)

NCT00922324Safety and Tolerability of STP206 in Healthy Adult Subjects

Phase 1

Valproic Acid

Spinal Muscular Atrophy

PHASE_1

STP206

Necrotizing Enterocolitis

PHASE_1

Clinical Trials (1)

NCT01954017STP206 for the Prevention of Necrotizing Enterocolitis (NEC)

Phase 1

Valproic Acid and Levocarnitine

Spinal Muscular Atrophy Type I

PHASE_1_2

Clinical Trials (1)

NCT00661453CARNIVAL Type I: Valproic Acid and Carnitine in Infants With Spinal Muscular Atrophy (SMA) Type I

Phase 1/2

Syntocinon Nasalspray

Female Sexual Dysfunction

PHASE_2

Clinical Trials (1)

NCT02229721Effect of Chronic Intranasal Oxytocin Administration on Sexual Function in Pre- and Postmenopausal Women

Phase 2

ManNAc

GNE Myopathy

PHASE_2

Methotrexate

Leukemia, Lymphocytic, Acute

PHASE_2

Clinical Trials (1)

NCT00905034Methotrexate, Vincristine, Pegylated L-Asparaginase and Dexamethasone (MOAD) in Acute Lymphoblastic Leukemia (ALL) Salvage

Phase 2

DNR

Acute Lymphocytic Leukemia

PHASE_2

Clinical Trials (1)

NCT02043587Chemotherapy With Liposomal Cytarabine CNS Prophylaxis for Adult Acute Lymphoblastic Leukemia & Lymphoblastic Lymphoma

Phase 2

Valproic Acid and Levocarnitine

Spinal Muscular Atrophy

PHASE_2

EZN-2279

ADA-SCID

PHASE_3

Clinical Trials (1)

NCT01420627EZN-2279 in Patients With ADA-SCID

Phase 3

acetyl-L-carnitine/statin

Diabetes Type 2

PHASE_3

Clinical Trials (1)

NCT00984750Acetyl-L-Carnitine in Type 2 Diabetes

Phase 3

Chenodeoxycholic acid

Cerebrotendinous Xanthomatoses

PHASE_3

Clinical Trials (1)

NCT06260748A Study of Chenodeoxycholic Acid (CDCA) in Newly Diagnosed Participants With Cerebrotendinous Xanthomatosis (CTX)

Phase 3

CHENODIOL

chenodiol

Post-LOE

ORAL · TABLET

CLINICAL PHARMACOLOGY At therapeutic doses, chenodiol suppresses hepatic synthesis of both cholesterol and cholic acid, gradually replacing the latter and its metabolite, deoxycholic acid in an expanded bile acid pool. These actions contribute to biliary cholesterol desaturation and gradual dissolution of radiolucent cholesterol gallstones in the presence of a gall-bladder visualized by oral cholecystography. Chenodiol has no effect on radiopaque (calcified) gallstones or on radiolucent bile pigment stones. Chenodiol is well absorbed from the small intestine and taken up by the liver where it is converted to its taurine and glycine conjugates and secreted in bile. Owing to 60 % to 80% first-pass hepatic clearance, the body pool of chenodiol resides mainly in the enterohepatic circulation; serum and urinary bile acid levels are not significantly affected during chenodiol therapy. At steady-state, an amount of chenodiol near the daily dose escapes to the colon and is converted by bacterial action to lithocholic acid. About 80% of the lithocholate is excreted in the feces; the remainder is absorbed and converted in the liver to its poorly absorbed sulfolithocholyl conjugates. During chenodiol therapy there is only a minor increase in biliary lithocholate, while fecal bile acids are increased three- to fourfold. Chenodiol is unequivocally hepatotoxic in many animal species, including sub-human primates at doses close to the human dose. Although the theoretical cause is the metabolite, lithocholic acid, an established hepatotoxin, and man has an efficient mechanism for sulfating and eliminating this substance, there is some evidence that the demonstrated hepatotoxicity is partly due to chenodiol per se . The hepatotoxicity of lithocholic acid is characterized biochemically and morphologically as cholestatic. Man has the capacity to form sulfate conjugates of lithocholic acid. Variation in this capacity among individuals has not been well established and a recent published report suggests that patients who develop chenodiol-induced serum aminotransferase elevations are poor sulfators of lithocholic acid ( see and ) . General Clinical Results: Both the desaturation of bile and the clinical dissolution of cholesterol gallstones are dose-related. In the National Cooperative Gallstone Study (NCGS) involving 305 patients in each treatment group, placebo and chenodiol dosages of 375 mg and 750 mg per day were associated with complete stone dissolution in 0.8%, 5.2% and 13.5%, respectively, of enrolled subjects over 24 months of treatment. Uncontrolled clinical trials using higher doses than those used in the NCGS have shown complete dissolution rates of 28 to 38% of enrolled patients receiving body weight doses of from 13 to 16 mg/kg/day for up to 24 months. In a prospective trial using 15 mg/kg/day, 31% enrolled surgical-risk patients treated more than six months (n = 86) achieved complete confirmed dissolutions. Observed stone dissolution rates achieved wi

2009

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