niacinamide has been researched along with Bilirubinemia in 8 studies
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.
| Excerpt | Relevance | Reference |
|---|---|---|
| " However, lapatinib (LAP), pazopanib (PAZ), regorafenib (REG) and sorafenib (SOR) have been implicated in the development of hyperbilirubinemia in patients." | 7.85 | Inhibition of human UDP-glucuronosyltransferase enzymes by lapatinib, pazopanib, regorafenib and sorafenib: Implications for hyperbilirubinemia. ( Burns, K; Chau, N; Kichenadasse, G; Knights, KM; Mackenzie, PI; McKinnon, RA; Miners, JO; Rowland, A; Tucker, GT, 2017) |
| "Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase)." | 7.78 | Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia. ( Dahut, W; English, BC; Federspiel, J; Figg, WD; Gardner, ER; Giaccone, G; Jain, L; Kim, A; Kirkland, CT; Kohn, E; Kummar, S; Peer, CJ; Richardson, ED; Sissung, TM; Troutman, SM; Venzon, D; Widemann, B; Woo, S; Yarchoan, R, 2012) |
| "To report a single case of uridine glucuronosyltransferase 1A1 (UGT1A1) polymorphism and hyperbilirubinemia in a patient who received sorafenib." | 7.75 | UGT1A1 polymorphism and hyperbilirubinemia in a patient who received sorafenib. ( Christensen, O; Chu, QS; Das, S; Meza-Junco, J; Rajagopalan, P; Sawyer, MB; Stefanyschyn, R, 2009) |
| " However, lapatinib (LAP), pazopanib (PAZ), regorafenib (REG) and sorafenib (SOR) have been implicated in the development of hyperbilirubinemia in patients." | 3.85 | Inhibition of human UDP-glucuronosyltransferase enzymes by lapatinib, pazopanib, regorafenib and sorafenib: Implications for hyperbilirubinemia. ( Burns, K; Chau, N; Kichenadasse, G; Knights, KM; Mackenzie, PI; McKinnon, RA; Miners, JO; Rowland, A; Tucker, GT, 2017) |
| "Several case reports suggest sorafenib exposure and sorafenib-induced hyperbilirubinemia may be related to a (TA)(5/6/7) repeat polymorphism in UGT1A1*28 (UGT, uridine glucuronosyl transferase)." | 3.78 | Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia. ( Dahut, W; English, BC; Federspiel, J; Figg, WD; Gardner, ER; Giaccone, G; Jain, L; Kim, A; Kirkland, CT; Kohn, E; Kummar, S; Peer, CJ; Richardson, ED; Sissung, TM; Troutman, SM; Venzon, D; Widemann, B; Woo, S; Yarchoan, R, 2012) |
| "To report a single case of uridine glucuronosyltransferase 1A1 (UGT1A1) polymorphism and hyperbilirubinemia in a patient who received sorafenib." | 3.75 | UGT1A1 polymorphism and hyperbilirubinemia in a patient who received sorafenib. ( Christensen, O; Chu, QS; Das, S; Meza-Junco, J; Rajagopalan, P; Sawyer, MB; Stefanyschyn, R, 2009) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 5 (62.50) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 1 (12.50) | 29.6817 |
| 2010's | 2 (25.00) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Miners, JO | 1 |
| Chau, N | 1 |
| Rowland, A | 1 |
| Burns, K | 1 |
| McKinnon, RA | 1 |
| Mackenzie, PI | 1 |
| Tucker, GT | 1 |
| Knights, KM | 1 |
| Kichenadasse, G | 1 |
| Meza-Junco, J | 1 |
| Chu, QS | 1 |
| Christensen, O | 1 |
| Rajagopalan, P | 1 |
| Das, S | 1 |
| Stefanyschyn, R | 1 |
| Sawyer, MB | 1 |
| Peer, CJ | 1 |
| Sissung, TM | 1 |
| Kim, A | 1 |
| Jain, L | 1 |
| Woo, S | 1 |
| Gardner, ER | 1 |
| Kirkland, CT | 1 |
| Troutman, SM | 1 |
| English, BC | 1 |
| Richardson, ED | 1 |
| Federspiel, J | 1 |
| Venzon, D | 1 |
| Dahut, W | 1 |
| Kohn, E | 1 |
| Kummar, S | 1 |
| Yarchoan, R | 1 |
| Giaccone, G | 1 |
| Widemann, B | 1 |
| Figg, WD | 1 |
| ESPOSITO, S | 1 |
| CALI, G | 1 |
| PIETROPAOLO, C | 1 |
| LOCOCO, G | 1 |
| Marini, A | 1 |
| Flauto, U | 1 |
| Careddu, P | 1 |
| Wilson, JT | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Phase II Study of BAY 43-9006 (Sorafenib) in Metastatic, Androgen-Independent Prostate Cancer[NCT00090545] | Phase 2 | 46 participants (Actual) | Interventional | 2004-09-01 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Geometric mean exposure for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose
| Intervention | mg/L.h (Geometric Mean) |
|---|---|
| First Stage - Disease Progression | 9.76 |
| Second Stage - Increased Accrual | 18.63 |
Plasma concentration-time profile for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, AND 24 hours post dose
| Intervention | mg/L (Mean) |
|---|---|
| First Stage - Disease Progression | 1.28 |
| Second Stage - Increased Accrual | 2.57 |
Time from treatment start date until date of death or date last known alive. (NCT00090545)
Timeframe: Time from treatment start date until date of death or date last known alive, approximately 18.3 months.
| Intervention | Months (Median) |
|---|---|
| First Stage - Disease Progression | 18 |
| Second Stage - Increased Accrual | 18.3 |
Here is the number of participants with adverse events. For the detailed list of adverse events, see the adverse event module. (NCT00090545)
Timeframe: Date treatment consent signed to date off study, approximately 49 months.
| Intervention | Participants (Count of Participants) |
|---|---|
| First Stage - Disease Progression | 22 |
| Second Stage - Increased Accrual | 23 |
Determine whether BAY 43-9006 when used to treat metastatic prostate cancer is associated with having 50% of Patients Progression Free at 4 Months by clinical, radiographic, and prostatic specific antigen (PSA)criteria. (NCT00090545)
Timeframe: 4 months
| Intervention | months (Median) |
|---|---|
| First Stage - Disease Progression | 1.83 |
| Second Stage - Increased Accrual | 3.7 |
Time to maximum concentration for sorafenib. (NCT00090545)
Timeframe: 0, 0.25, 0.50, 1, 2, 4, 6, 8, 12, and 24 hours post-dose
| Intervention | hours (Median) |
|---|---|
| First Stage - Disease Progression | 0.68 |
| Second Stage - Increased Accrual | 8 |
Overall response was evaluated by the RECIST. Complete Response (CR) is the disappearance of all target lesions. Partial Response (PR) is at least a 30% decrease in the sum of the diameters of target lesions, taking as reference the baseline sum diameters. Progressive Disease (PD) is at least a 20% increase in the sum of the diameters of target lesions, taking as reference the smallest sum on study. Stable Disease (SD) is neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum diameters while on study. (NCT00090545)
Timeframe: Every 2 cycles (1 cycle = 28 days)
| Intervention | Participants (Count of Participants) | |||
|---|---|---|---|---|
| Complete Response | Partial Response | Progressive Disease | Stable Disease | |
| First Stage - Disease Progression | 0 | 0 | 8 | 0 |
| Second Stage - Increased Accrual | 0 | 1 | 13 | 10 |
1 review available for niacinamide and Bilirubinemia
| Article | Year |
|---|---|
Developmental pharmacology: a review of its application to clinical and basic science.
Topics: Aging; Androgens; Aniline Compounds; Animals; Estrogens; Ethanol; Female; Fetus; Fluorosis, Dental; | 1972 |
1 trial available for niacinamide and Bilirubinemia
| Article | Year |
|---|---|
Nicotinic acid in the treatment of schizophrenia.
Topics: Acute Disease; Blood Glucose; Chronic Disease; Clinical Trials as Topic; Humans; Hyperbilirubinemia; | 1973 |
6 other studies available for niacinamide and Bilirubinemia
| Article | Year |
|---|---|
Inhibition of human UDP-glucuronosyltransferase enzymes by lapatinib, pazopanib, regorafenib and sorafenib: Implications for hyperbilirubinemia.
Topics: Bilirubin; Catalysis; Enzyme Inhibitors; Glucuronosyltransferase; Humans; Hyperbilirubinemia; Indazo | 2017 |
UGT1A1 polymorphism and hyperbilirubinemia in a patient who received sorafenib.
Topics: Antineoplastic Combined Chemotherapy Protocols; Benzenesulfonates; Carcinoma, Hepatocellular; Clinic | 2009 |
Sorafenib is an inhibitor of UGT1A1 but is metabolized by UGT1A9: implications of genetic variants on pharmacokinetics and hyperbilirubinemia.
Topics: Aged; Antineoplastic Agents; Area Under Curve; Benzenesulfonates; Bilirubin; Clinical Trials as Topi | 2012 |
[The action of nicotinamide and nicotinic acid on hemopoiesis and hemocatheresis. The behavior of sideremia and bilirubinemia in normal and splenectomized animals treated with nicotinic acid].
Topics: Animals; Bilirubin; Hematopoiesis; Hyperbilirubinemia; Iron; Niacin; Niacinamide; Nicotinic Acids | 1960 |
[INFLUENCE OF SUBSTANCES WITH A PYRIDINE NUCLEUS ON SIDEREMIC AND BILIRUBINEMIC LEVELS].
Topics: Bilirubin; Blood; Hyperbilirubinemia; Iron; Niacin; Niacinamide; Nicotinic Acids; Pharmacology; Pyri | 1964 |
[Administration of uridinediphosphoglucose (UDPG) and behavior of blood bilirubin in the newborn].
Topics: Bilirubin; Diseases in Twins; Glucose; Humans; Hyperbilirubinemia; Infant, Newborn; Infant, Prematur | 1969 |