Details
| Stereochemistry | ABSOLUTE |
| Molecular Formula | C26H32N2O4 |
| Molecular Weight | 436.5433 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CC(C)(CC1CC2=C(C1)C=CC=C2)NC[C@@H](O)COC3=C(C=CC(CCC(O)=O)=C3)C#N
InChI
InChIKey=NJBFJCJKWWIKRD-HSZRJFAPSA-N
InChI=1S/C26H32N2O4/c1-26(2,14-19-11-20-5-3-4-6-21(20)12-19)28-16-23(29)17-32-24-13-18(8-10-25(30)31)7-9-22(24)15-27/h3-7,9,13,19,23,28-29H,8,10-12,14,16-17H2,1-2H3,(H,30,31)/t23-/m1/s1
| Molecular Formula | C26H32N2O4 |
| Molecular Weight | 436.5433 |
| Charge | 0 |
| Count |
|
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
Approval Year
| Substance Class |
Chemical
Created
by
admin
on
Edited
Mon Mar 31 20:38:17 GMT 2025
by
admin
on
Mon Mar 31 20:38:17 GMT 2025
|
| Record UNII |
615K7YBS59
|
| Record Status |
Validated (UNII)
|
| Record Version |
|
-
Download
| Name | Type | Language | ||
|---|---|---|---|---|
|
Common Name | English | ||
|
Preferred Name | English | ||
|
Code | English | ||
|
Systematic Name | English | ||
|
Common Name | English | ||
|
Code | English | ||
|
Code | English | ||
|
Systematic Name | English |
| Code System | Code | Type | Description | ||
|---|---|---|---|---|---|
|
SB-423562
Created by
admin on Mon Mar 31 20:38:17 GMT 2025 , Edited by admin on Mon Mar 31 20:38:17 GMT 2025
|
PRIMARY | NPS Pharmaceuticals (NASDAQ: NPSP) has initiated a Phase 2a study to evaluate the safety and tolerability of NPSP795 in adult patients with Autosomal Dominant Hypocalcemia (ADH), an ultra-rare genetic disorder of calcium homeostasis. ADH is caused by mutations of the calcium-sensing receptor (CaSR) gene that increase the sensitivity of the receptor to serum calcium. NPSP795 is a selective calcium receptor antagonist, which binds to the CaSR and decreases its sensitivity to serum calcium. Its mechanism of action is believed to restore the normal physiological action of the CaSR and address the underlying molecular defect in ADH to return to normal calcium homeostasis. The company expects to report preliminary top-line data from the study in late 2014 or early 2015. | ||
|
615K7YBS59
Created by
admin on Mon Mar 31 20:38:17 GMT 2025 , Edited by admin on Mon Mar 31 20:38:17 GMT 2025
|
PRIMARY | |||
|
351490-27-2
Created by
admin on Mon Mar 31 20:38:17 GMT 2025 , Edited by admin on Mon Mar 31 20:38:17 GMT 2025
|
PRIMARY | |||
|
9910902
Created by
admin on Mon Mar 31 20:38:17 GMT 2025 , Edited by admin on Mon Mar 31 20:38:17 GMT 2025
|
PRIMARY |
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
SALT/SOLVATE -> PARENT |
|
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
PRODRUG -> METABOLITE ACTIVE |
| Related Record | Type | Details | ||
|---|---|---|---|---|
|
ACTIVE MOIETY |
Chronic administration of SB-423557 did not increase parathyroid cell proliferation in rats. In healthy human volunteers, single doses of intravenous SB-423562 and oral SB-423557 elicited transient elevations of endogenous PTH concentrations in a profile similar to that observed with subcutaneously administered PTH. Both agents were well tolerated in humans. Transient increases in serum calcium, an expected effect of increased parathyroid hormone concentrations, were observed post-dose at the higher doses of SB-423557 studied. These data constitute an early proof of principle in humans and provide the basis for further development of this class of compound as a novel, orally administered bone-forming treatment for osteoporosis.
|
