U.S. Department of Health & Human Services Divider Arrow National Institutes of Health Divider Arrow NCATS

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

    {{facet.count}}
    {{facet.count}}

Showing 21 - 30 of 42 results

Status:
US Previously Marketed
Source:
Pabalate by Robins
(1949)
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)



AMINOBENZOATE SODIUM is a salt of Aminobenzoic acid. Aminobenzoic acid is an intermediate in the synthesis of folate by bacteria, plants, and fungi. Many bacteria, including those found in the human intestinal tract such as E. coli, generate Aminobenzoic acid from chorismate by the combined action of the enzymes 4-amino-4-deoxychorismate synthase and 4-amino-4-deoxychorismate lyase. Plants produce Aminobenzoic acid in their chloroplasts, and store it as a glucose ester (pABA-Glc) in their tissues. Humans lack the enzymes to convert Aminobenzoic acid to folate, so require folate from dietary sources such as green leafy vegetables. In humans, Aminobenzoic acid is considered nonessential and, although it has been referred to historically as "vitamin Bx", is no longer recognized as a vitamin, because most people have colon bacteria that generate Aminobenzoic acid. The potassium salt is used as a drug against fibrotic skin disorders, such as Peyronie's disease, under the trade name Potaba.
Status:
US Previously Marketed
Source:
Hytakerol by Winthrop-Stearns (Winthrop)
(1940)
Source URL:
First approved in 1940
Source:
Hytakerol by Winthrop-Stearns (Winthrop)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)



Dihydrotachysterol (DHT) is a synthetic vitamin D analog activated in the liver that does not require renal hydroxylation like vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). Dihydrotachysterol is used to treat hypocalcemia, hypoparathyroidism, and prevention of tetany. Dihydrotachysterol is hydroxylated in the liver to 25-hydroxy-dihydrotachysterol, which is the major circulating active form of the drug. Once hydroxylated to 25-hydroxy-dihydrotachysterol, the modified drug binds to the vitamin D receptor. The bound form of the vitamin D receptor serves as a transcriptional regulator of bone matrix proteins, inducing the expression of osteocalcin and suppressing synthesis of type I collagen. Dihydrotachysterol also increases renal phosphate excretion.
Status:
Possibly Marketed Outside US
Source:
NCT00960973: Phase 4 Interventional Completed Diabetes
(2009)
Source URL:
First approved in 2023
Source:
Anti aging by XIAN CHIANG COMPANY LIMITED
Source URL:

Class (Stereo):
CHEMICAL (ACHIRAL)


Conditions:

Menatetrenone (INN), also known as MK4, is a vitamin K compound used as a hemostatic agent, and also as adjunctive therapy for the pain of osteoporosis. MK4 is marketed for the osteoporosis indication in Japan by Eisai Co., under the trade name Glakay. Has several mechanism of actions: (1) Acceleration of osteogenesis. In human osteoblast cultures, calcification was accelerated by administration of menatetrenone at a concentration of 2.25 × 10-6 mol/L alone or when it was coadministered with 1,25(OH)2D3. The osteocalcin content in the cell layers was increased by coadministration with 1,25(OH)2D3. 2. Inhibition of bone resorption. In organ cultures of mouse calvaria, at concentrations of 3 × 10-6 to 3 × 10-5 mol/L, menatetrenone inhibited bone resorption induced by IL-1α, PGE2, PTH and 1,25(OH)2D3. In mouse bone marrow cell cultures, at concentrations of 3 × 10-6 to 1 × 10-5 mol/L, menatetrenone inhibited the induction of osteoclast release by 1,25(OH)2D3. 3. Effect on serum level of osteocalcin. Menatetrenone was administered to patients with osteoporosis at a dose of 45 mg/day for 2 years. Menatetrenone increased the serum level of osteocalcin and decreased the serum level of Glu-osteocalcin.
Status:
Possibly Marketed Outside US
Source:
Flavitan by Warburg, O.|Christian, W.
Source URL:
First approved in 2011

Class (Stereo):
CHEMICAL (ABSOLUTE)



Flavin adenine dinucleotide is a coenzyme form of vitamin B2. Many oxidoreductases, called flavoenzymes or flavoproteins, require FAD as a prosthetic group, which functions in electron transfers. It is usually used for the prevention and treatment of various diseases that are caused by Vitamin B2 deficiency or metabolic disorder including stomatitis, eczema, etc. No adverse reactions were reported.
Status:
Possibly Marketed Outside US
Source:
CURATODERM by Teijin Pharma
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Conditions:

Talcalcitol is a synthetic analogue of vitamin D3. Tacalcitol has been developed by Teijin in Japan with the aim of maintaining the potent cell-regulating properties of calcitriol without the calcium-related adverse effects. Tacalcitol differs structurally from calcitriol by hydroxylation in the 24 position instead of the 25 position. Tacalcitol can influence the principal pathogenetic factors of psoriasis by inducing normalisation of keratinocyte differentiation, performing an anti-proliferative action and finally modulating the inflammatory response. Tacalcitol has been launched as an ointment formulation for the treatment of psoriasis in various countries. High-dose formulations (ointment and lotion) are available in Japan.
Status:
Possibly Marketed Outside US
Source:
Japan:Secalciferol
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Conditions:

Secalciferol (24,25-DIHYDROXYVITAMIN D 3/24R,25(OH)(2)D(3)) is suggested to be an essential hormone for the process of bone fracture healing, it has a physiological role in human bone and mineral metabolism, leading to an enhancement of osteocalcin synthesis. Secalciferol is possibly to bind a nuclear protein vitamin D receptor (VDR) to the ligand binding domain, which is stereo-specific for Secalciferol. The downstream effect will be triggered after the binding, including the inhibition of calcium channel to regulate the calcium homeostasis, and the following reduction of p53 and Pi-induced cytochrome C translocation
Status:
Possibly Marketed Outside US
Source:
EDIROL by Chugai Pharmaceutical
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Conditions:

Eldecalcitol (1α, 25-dihydroxy-2β-[3-hydroxypropyloxy] vitamin D3; ED-71) is an analog of the active form of vitamin D. Eldecalcitol has a hydroxypropyloxy group at the 2β-position of 1,25(OH)2D3. Compared with 1,25(OH)2D3, eldecalcitol has a higher affinity for serum vitamin D-binding protein (DBP), binds more weakly to vitamin D receptor, and shows lower potency in suppression of serum parathyroid hormone. The plasma half-life of eldecalcitol is longer than that of 1,25(OH)2D3, probably due to the higher affinity for DBP. In addition to regulation of calcium metabolism carried out by conventional vitamin D analogs, eldecalcitol possesses a strong inhibitory effect on bone resorption and causes a significant increase in bone mineral density. EDIROL (Eldecalcitol) has been approved for the treatment of osteoporosis in Japan.
Status:
Possibly Marketed Outside US
Source:
NCT02868203: Phase 4 Interventional Unknown status Angina, Unstable
(2016)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)



Maxacalcitol (OXAROL®) is a derivative of vitamin D and is used to treat the secondary hyperparathyroidism of hemodialysis (HD) patients as an injection and psoriasis as an ointment. Secondary hyperparathyroidism is one of the complications in HD patients with hyperplasia of parathyroid glands and elevated serum parathyroid hormone (PTH) levels. Maxacalcitol (OXAROL®) suppresses synthesis and secretion of parathyroid hormone, and decreases a concentration of parathyroid hormone in blood. It also inhibits proliferation and induces differentiation of epidermal keratinocytes. Maxacalcitol (OXAROL®) used in patients with keratosis including psoriasis vulgaris, remarkably improving the symptoms.
Status:
Possibly Marketed Outside US
Source:
NCT03210688: Phase 4 Interventional Completed Minimal Change Disease
(2018)
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)



Alfacalcidol (1-hydroxyvitamin D3) is a synthetic analog of vitamin D introduced clinically in the early 1970s. A prodrug for calcitriol (1,25-dihydroxyvitamin D3), it is one of the most potent and rapidly acting compounds currently used in the prevention and treatment of vitamin D deficiency states and hypocalcemia. The clinical benefit of alfacalcidol is related to the stimulation of calcium and phosphorus absorption, reversal of myopathy, promotion of mineralization in bone and the ability to reabsorb fully mineralized bone. Similar marketed vitamin D compounds include calcitriol and ergocalciferol. Alfacalcidol is indicated in conditions where there is a disturbance of calcium metabolism due to impaired 1-α hydroxylation such as when there is reduced renal function.
Status:
Possibly Marketed Outside US
Source:
Hornel by University of Wisconsin-Madison
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)


Falecalcitriol is an analog of calcitriol. Falecalcitriol was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on Apr 4, 2001. It was co-developed by Taisho, Dainippon Sumitomo and Kissei, then marketed as Hornel by Taisho and Taisho Toyama or as Fulstan by Dainippon Sumitomo Pharma and Kissei in JP. It has a higher potency both in vivo and in vitro systems, and longer duration of action in vivo. This medicine improves bone disease and symptoms caused by shortage of vitamin D, etc. It also prompts calcium absorption to supply lacked calcium and prevents bone-thinning. It is usually used to treat secondary hyperparathyroidism under maintenance dialysis, hypoparathyroidism, rickets or osteomalacia. Falecalcitriol regulates the proliferation of parathyroid cells and parathyroid hormone synthesis possibly via binding to a nuclear receptor for vitamin D (VDR). It is often not possible to administer doses high enough to sufficiently inhibit parathyroid hormones because of the risk of hypercalcemia and hyperphosphatemia.

Showing 21 - 30 of 42 results