2,3-diphosphoglycerate has been researched along with HbS Disease in 36 studies
2,3-Diphosphoglycerate: A highly anionic organic phosphate which is present in human red blood cells at about the same molar ratio as hemoglobin. It binds to deoxyhemoglobin but not the oxygenated form, therefore diminishing the oxygen affinity of hemoglobin. This is essential in enabling hemoglobin to unload oxygen in tissue capillaries. It is also an intermediate in the conversion of 3-phosphoglycerate to 2-phosphoglycerate by phosphoglycerate mutase (EC 5.4.2.1). (From Stryer Biochemistry, 4th ed, p160; Enzyme Nomenclature, 1992, p508)
2,3-bisphosphoglyceric acid : A bisphosphoglyceric acid that is glyceric acid carrying two phospho substituents at positions 2 and 3.
| Excerpt | Relevance | Reference |
|---|---|---|
| " When animals lacking 2,3-DPG were dosed with a compound designed to increase hemoglobin oxygen affinity, oxygen delivery related toxicity was observed." | 1.91 | Effects of 2,3-DPG knockout on SCD phenotype in Townes SCD model mice. ( Ahn, Y; Barakat, A; Field, D; Jasuja, R; Kapinos, B; Knee, KM; Lintner, N; Pagan, V; Petterson, BA; Ramaiah, L; Sawant, A; Tomlinson, L; Wenzel, Z, 2023) |
| " After daily dosing of etavopivat over 5 consecutive days in NHPs, ATP was increased by 38% from baseline." | 1.72 | Etavopivat, a Pyruvate Kinase Activator in Red Blood Cells, for the Treatment of Sickle Cell Disease. ( Drake, A; Fessler, R; Forsyth, S; Fulzele, K; Guichard, S; Kalfa, TA; Konstantinidis, DG; Marshall, CG; Ribadeneira, MD; Schroeder, P; Seu, KG; Wilker, E, 2022) |
| "Hydroxyurea was associated with significantly shorter TSpO2 < 88 (P = 0." | 1.43 | Dense red blood cell and oxygen desaturation in sickle-cell disease. ( Bartolucci, P; Boyer, L; Conti, M; Di Liberto, G; Galacteros, F; Habibi, A; Khorgami, S; Kiger, L; Maitre, B; Marden, MC; Pirenne, F; Poitrine, FC; Rakotoson, MG; Vingert, B, 2016) |
| " I hypothesize that NO may suppress BPG production by (1) inhibiting glyceraldehyde-3-phosphate dehydrogenase (G3PDH), the most critical glycolytic enzyme for the bioavailability of 1,3-bisphosphoglycerate; and to a lesser extent by (2) associated pH changes in the deoxy-Hb-catalyzed depletion of nitrite, a metabolic reservoir of NO." | 1.38 | Nitric oxide-mediated suppression of 2,3-bisphosphoglycerate synthesis: therapeutic relevance for environmental hypoxia and sickle cell disease. ( Bertrand, R, 2012) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 14 (38.89) | 18.7374 |
| 1990's | 7 (19.44) | 18.2507 |
| 2000's | 3 (8.33) | 29.6817 |
| 2010's | 6 (16.67) | 24.3611 |
| 2020's | 6 (16.67) | 2.80 |
| Authors | Studies |
|---|---|
| Schroeder, P | 1 |
| Fulzele, K | 1 |
| Forsyth, S | 1 |
| Ribadeneira, MD | 1 |
| Guichard, S | 1 |
| Wilker, E | 1 |
| Marshall, CG | 1 |
| Drake, A | 1 |
| Fessler, R | 1 |
| Konstantinidis, DG | 1 |
| Seu, KG | 1 |
| Kalfa, TA | 1 |
| Wang, X | 2 |
| Gardner, K | 1 |
| Tegegn, MB | 1 |
| Dalgard, CL | 1 |
| Alba, C | 1 |
| Menzel, S | 1 |
| Patel, H | 1 |
| Pirooznia, M | 1 |
| Fu, YP | 1 |
| Seifuddin, FT | 1 |
| Thein, SL | 2 |
| Quezado, ZMN | 1 |
| Kamimura, S | 1 |
| Smith, M | 1 |
| Heaven, MR | 1 |
| Jana, S | 1 |
| Vogel, S | 1 |
| Zerfas, P | 1 |
| Combs, CA | 1 |
| Almeida, LEF | 1 |
| Li, Q | 2 |
| Quezado, M | 1 |
| Horkayne-Szakaly, I | 1 |
| Kosinski, PA | 3 |
| Yu, S | 1 |
| Kapadnis, U | 1 |
| Kung, C | 3 |
| Dang, L | 3 |
| Wakim, P | 1 |
| Eaton, WA | 2 |
| Alayash, AI | 1 |
| Xu, JZ | 1 |
| Conrey, A | 1 |
| Frey, I | 1 |
| Gwaabe, E | 1 |
| Menapace, LA | 1 |
| Tumburu, L | 1 |
| Lundt, M | 1 |
| Lequang, T | 1 |
| Glass, K | 1 |
| Dunkelberger, EB | 1 |
| Iyer, V | 1 |
| Mangus, H | 2 |
| Hawkins, P | 1 |
| Jeffries, N | 1 |
| Lay Thein, S | 1 |
| Barakat, A | 1 |
| Jasuja, R | 1 |
| Tomlinson, L | 1 |
| Wenzel, Z | 1 |
| Ramaiah, L | 1 |
| Petterson, BA | 1 |
| Kapinos, B | 1 |
| Sawant, A | 1 |
| Pagan, V | 1 |
| Lintner, N | 1 |
| Field, D | 1 |
| Ahn, Y | 1 |
| Knee, KM | 1 |
| Rab, MAE | 1 |
| Bos, J | 1 |
| van Oirschot, BA | 1 |
| van Straaten, S | 1 |
| Chubukov, V | 1 |
| Kim, H | 1 |
| Schutgens, REG | 1 |
| Pasterkamp, G | 1 |
| van Beers, EJ | 1 |
| van Wijk, R | 1 |
| Sun, K | 1 |
| D'Alessandro, A | 1 |
| Ahmed, MH | 1 |
| Zhang, Y | 2 |
| Song, A | 2 |
| Ko, TP | 1 |
| Nemkov, T | 1 |
| Reisz, JA | 1 |
| Wu, H | 1 |
| Adebiyi, M | 2 |
| Peng, Z | 1 |
| Gong, J | 1 |
| Liu, H | 2 |
| Huang, A | 1 |
| Wen, YE | 2 |
| Wen, AQ | 2 |
| Berka, V | 1 |
| Bogdanov, MV | 1 |
| Abdulmalik, O | 1 |
| Han, L | 1 |
| Tsai, AL | 1 |
| Idowu, M | 2 |
| Juneja, HS | 2 |
| Kellems, RE | 2 |
| Dowhan, W | 1 |
| Hansen, KC | 1 |
| Safo, MK | 1 |
| Xia, Y | 3 |
| Hebbel, RP | 1 |
| Hedlund, BE | 1 |
| Liu, RR | 1 |
| Manalo, J | 1 |
| Weng, T | 1 |
| Ko, J | 1 |
| Eltzschig, HK | 1 |
| Blackburn, MR | 1 |
| Di Liberto, G | 1 |
| Kiger, L | 1 |
| Marden, MC | 1 |
| Boyer, L | 1 |
| Poitrine, FC | 1 |
| Conti, M | 1 |
| Rakotoson, MG | 1 |
| Habibi, A | 1 |
| Khorgami, S | 1 |
| Vingert, B | 1 |
| Maitre, B | 1 |
| Galacteros, F | 1 |
| Pirenne, F | 1 |
| Bartolucci, P | 1 |
| Bertrand, R | 1 |
| Willcocks, JP | 1 |
| Mulquiney, PJ | 1 |
| Ellory, JC | 1 |
| Veech, RL | 1 |
| Radda, GK | 1 |
| Clarke, K | 1 |
| Sarode, R | 1 |
| Altuntas, F | 1 |
| Perutz, MF | 1 |
| Poyart, C | 1 |
| Roth, EF | 1 |
| Nagel, RL | 2 |
| Bookchin, RM | 3 |
| Ueda, Y | 1 |
| Beddell, CR | 1 |
| Goodford, PJ | 1 |
| Kneen, G | 1 |
| White, RD | 1 |
| Wilkinson, S | 1 |
| Wootton, R | 1 |
| Lachant, NA | 2 |
| Davidson, WD | 1 |
| Tanaka, KR | 2 |
| Castro, O | 3 |
| Tehrani, AY | 1 |
| Lam, YF | 1 |
| Lin, AK | 1 |
| Dosch, SF | 1 |
| Ho, C | 1 |
| Kumpati, J | 1 |
| Franco, RS | 1 |
| Weiner, M | 1 |
| Martelo, OJ | 1 |
| Poillon, WN | 5 |
| Kim, BC | 4 |
| Labotka, RJ | 1 |
| Hicks, CU | 1 |
| Kark, JA | 1 |
| McCune, SL | 1 |
| Reilly, MP | 2 |
| Chomo, MJ | 1 |
| Asakura, T | 2 |
| Townes, TM | 1 |
| Ould Amar, AK | 1 |
| Kérob-Bauchet, B | 1 |
| Robert, P | 1 |
| Leconte, C | 1 |
| Maier, H | 1 |
| Bera, O | 1 |
| Plumelle, Y | 1 |
| Hyronimus, JC | 1 |
| Césaire, R | 1 |
| Uchida, K | 1 |
| Rackoff, WR | 1 |
| Ohene-Frempong, K | 1 |
| Kim, HC | 1 |
| Fabry, ME | 1 |
| Suzuka, SM | 1 |
| Weinberg, RS | 1 |
| Lawrence, C | 1 |
| Factor, SM | 1 |
| Gilman, JG | 1 |
| Costantini, F | 1 |
| Ortiz, OE | 1 |
| Lew, VL | 1 |
| Bayoumi, RA | 1 |
| Abu Zeid, YA | 1 |
| Abdul Sadig, A | 1 |
| Awad Elkarim, O | 1 |
| Adekile, AD | 1 |
| Zerez, CR | 1 |
| Welty, EV | 1 |
| Walder, JA | 1 |
| Briguglio, F | 1 |
| Briguglio, E | 1 |
| Di Marco, V | 1 |
| Rana, SR | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| A Pilot Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Escalating Multiple Oral Doses of AG-348 in Subjects With Stable Sickle Cell Disease[NCT04000165] | Early Phase 1 | 17 participants (Actual) | Interventional | 2019-07-11 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
To assess the clinical safety and tolerability of multiple escalating doses of AG-348, an allosteric activator of the enzyme pyruvate kinase, in subjects with stable sickle cell disease (SCD). Safety and tolerability were assessed by defined as a ≥ 1 g/dL increase in hemoglobin at any dose level compared to baseline. (NCT04000165)
Timeframe: 14 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| AG-348 in Participants With Sickle Cell Disease | 9 |
To assess the clinical safety and tolerability of multiple escalating doses of AG-348, an allosteric activator of the enzyme pyruvate kinase, in subjects with stable sickle cell disease (SCD). Safety and tolerability were assessed by frequency and severity of adverse events (AEs) using Common Terminology Criteria for Adverse Events (CTCAE) 5.0. (NCT04000165)
Timeframe: 14 weeks
| Intervention | Participants (Count of Participants) |
|---|---|
| AG-348 in Participants With Sickle Cell Disease | 2 |
To assess change in absolute reticulocyte count in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | K/mcL (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 196.44 | -20.97 | -20.72 | -44.99 | -34.1 | -13.77 | 8.1 |
To assess change in aspartate aminotransferase (AST) in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | U/L (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 33.88 | -3.31 | -3.37 | -2 | -3.54 | -2.49 | 3.02 |
To assess the change in fetal hemoglobin (HbF) in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | Percent HbF (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 20.39 | -0.42 | -1.02 | -1.31 | -0.34 | 0.19 | 0.81 |
To assess change in hemoglobin in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | g/dL (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 8.73 | 0.34 | 0.76 | 1.19 | 0.92 | 0.34 | 0.37 |
To assess change in lactic acid dehydrogenase (LDH) in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | U/L (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 348.4 | -7.81 | -39.94 | -25.31 | -37.89 | 20.63 | 30.72 |
To assess change in mean corpuscular volume (MCV) in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | fL (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 103.32 | -0.5 | 0.52 | 0.42 | 1.98 | -0.25 | -0.64 |
To assess change in total bilirubin in stable sickle cell disease participants at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | mg/dL (Mean) | ||||||
|---|---|---|---|---|---|---|---|
| Baseline | 5 mg dose of AG-348 | 20 mg dose AG-348 | 50 mg dose AG-348 | 100 mg dose AG-348 | End Of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 1.82 | -0.19 | -0.56 | -0.77 | -0.87 | -0.19 | 0.1 |
To assess the clinical safety and tolerability of multiple escalating doses of AG-348, an allosteric activator of the enzyme pyruvate kinase, in subjects with stable sickle cell disease (SCD). Safety and tolerability were assessed by frequency and severity of adverse events (AEs) using Common Terminology Criteria for Adverse Events (CTCAE) 5.0. (NCT04000165)
Timeframe: 14 weeks
| Intervention | Participants (Count of Participants) | ||
|---|---|---|---|
| Insomnia | Arthralgia | Hypertension | |
| AG-348 in Participants With Sickle Cell Disease | 6 | 3 | 3 |
Measure percent change from baseline in oxygen binding p50 value at each dose level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | Percent Change (Mean) | |||||
|---|---|---|---|---|---|---|
| 5 mg Dose AG-348 | 20 mg Dose AG-348 | 50 mg Dose AG-348 | 100 mg Dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 0.5 | -2.09 | -3.84 | -4.88 | 7.97 | 10.79 |
To understand the mechanisms of action of AG- 348 on the glycolytic pathway in sickle cell disease through laboratory studies of specific pharmacodynamics of 2,3-DPG at each dose level of AG-348. (NCT04000165)
Timeframe: 14 weeks
| Intervention | percent change (Mean) | |||||
|---|---|---|---|---|---|---|
| 5 mg Dose AG-348 | 20 mg Dose AG-348 | 50 mg Dose AG-348 | 100 mg Dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | -3.74 | -16.08 | -23.49 | -24.13 | 1.97 | 9.11 |
To understand the mechanisms of action of AG- 348 on the glycolytic pathway in sickle cell disease through laboratory studies of specific pharmacodynamics of adenosine triphosphate (ATP) at each dose level of AG-348. (NCT04000165)
Timeframe: 14 weeks
| Intervention | percent change (Mean) | |||||
|---|---|---|---|---|---|---|
| 5 mg Dose AG-348 | 20 mg Dose AG-348 | 50 mg Dose AG-348 | 100 mg Dose AG-348 | End of Taper Dose AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | 13.68 | 26.95 | 33.43 | 39.84 | 15.51 | 12.03 |
Measure percent change in Time (mins) at which 50% of red blood cells are sickled (t50) Value at Each Dose Level of AG-348 (NCT04000165)
Timeframe: 14 weeks
| Intervention | percent change (Mean) | |||||
|---|---|---|---|---|---|---|
| 5 mg Dose AG-348 | 20 mg Dose AG-348 | 50 mg Dose AG-348 | 100 mg Dose AG-348 | End of Taper AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | -0.46 | 10.19 | 7.11 | 13.98 | -11.38 | 1.67 |
To understand the mechanisms of action of AG- 348 on the glycolytic pathway in sickle cell disease through laboratory studies of specific pharmacodynamics of PK-R at each dose level of AG-348. (NCT04000165)
Timeframe: 14 weeks
| Intervention | percent change (Mean) | |||||
|---|---|---|---|---|---|---|
| 5 mg Dose AG-348 | 20 mg Dose AG-348 | 50 mg Dose AG-348 | 100 mg Dose AG-348 | End of Taper AG-348 | End of Study AG-348 | |
| AG-348 in Participants With Sickle Cell Disease | -6.89 | -2.82 | -10.66 | -28.99 | -8.38 | -16.47 |
2 reviews available for 2,3-diphosphoglycerate and HbS Disease
| Article | Year |
|---|---|
Adenosine signaling in normal and sickle erythrocytes and beyond.
Topics: 2,3-Diphosphoglycerate; Adenosine; Anemia, Sickle Cell; Animals; Erythrocytes; Erythrocytes, Abnorma | 2012 |
Blood bank issues associated with red cell exchanges in sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Black or African American; Bloo | 2006 |
3 trials available for 2,3-diphosphoglycerate and HbS Disease
| Article | Year |
|---|---|
A phase 1 dose escalation study of the pyruvate kinase activator mitapivat (AG-348) in sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Adult; Anemia, Sickle Cell; Hemoglobins; Humans; Pyr | 2022 |
Assessment of qualitative functional parameters of stored red blood cells from donors with sickle cell trait (AS) or with heterozygote (AC) status.
Topics: 2,3-Diphosphoglycerate; Adolescent; Adult; Aged; Anemia, Sickle Cell; Blood Donors; Blood Preservati | 1996 |
Effect of erythrocytapheresis on arterial oxygen saturation and hemoglobin oxygen affinity in patients with sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Adolescent; Adult; Anemia, Sickle Cell; Arteries; Blood Component Removal; B | 1998 |
31 other studies available for 2,3-diphosphoglycerate and HbS Disease
| Article | Year |
|---|---|
Etavopivat, a Pyruvate Kinase Activator in Red Blood Cells, for the Treatment of Sickle Cell Disease.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Animals; Erythrocytes; Hemoglob | 2022 |
Genetic variants of PKLR are associated with acute pain in sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Acute Pain; Adult; Anemia, Sickle Cell; Child; Erythrocytes, Abnormal; Hemog | 2022 |
Mitapivat increases ATP and decreases oxidative stress and erythrocyte mitochondria retention in a SCD mouse model.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Animals; Disease Models, Animal | 2022 |
Effects of 2,3-DPG knockout on SCD phenotype in Townes SCD model mice.
Topics: 2,3-Diphosphoglycerate; Adult; Anemia, Sickle Cell; Animals; Hemoglobins; Humans; Mice; Oxygen; Phen | 2023 |
Decreased activity and stability of pyruvate kinase in sickle cell disease: a novel target for mitapivat therapy.
Topics: 2,3-Diphosphoglycerate; Adolescent; Adult; Anemia, Sickle Cell; Cell Shape; Child; Child, Preschool; | 2021 |
Structural and Functional Insight of Sphingosine 1-Phosphate-Mediated Pathogenic Metabolic Reprogramming in Sickle Cell Disease.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Animals; Erythrocytes, Abnormal; Female; Hemoglobin A; | 2017 |
Sickle hemoglobin oxygen affinity-shifting strategies have unequal cerebrovascular risks.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Benzaldehydes; Cerebrovascular Circulation; Cerebrovasc | 2018 |
Elevated ecto-5'-nucleotidase: a missing pathogenic factor and new therapeutic target for sickle cell disease.
Topics: 2,3-Diphosphoglycerate; 5'-Nucleotidase; Adenosine; Adenosine Triphosphate; AMP-Activated Protein Ki | 2018 |
Dense red blood cell and oxygen desaturation in sickle-cell disease.
Topics: 2,3-Diphosphoglycerate; Adult; Aged; Aged, 80 and over; Anemia, Sickle Cell; Erythrocytes; Erythrocy | 2016 |
Nitric oxide-mediated suppression of 2,3-bisphosphoglycerate synthesis: therapeutic relevance for environmental hypoxia and sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Humans; Hypoxia; Models, Theoretical; Nitric Oxide | 2012 |
Simultaneous determination of low free Mg2+ and pH in human sickle cells using 31P NMR spectroscopy.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Erythrocytes; Hemoglobins; Huma | 2002 |
Bezafibrate lowers oxygen affinity of haemoglobin.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Bezafibrate; Clofibrate; Diphosphoglyceric Acids; Drug | 1983 |
pH dependency of potassium efflux from sickled red cells.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Cell Membrane Permeability; Diphosphoglyceric Acids; Er | 1981 |
Effects of carbon dioxide and pH variations in vitro on blood respiratory functions, red blood cell volume, transmembrane pH gradients, and sickling in sickle cell anemia.
Topics: 2,3-Diphosphoglycerate; Acidosis, Respiratory; Anemia, Sickle Cell; Carbon Dioxide; Diphosphoglyceri | 1984 |
Substituted benzaldehydes designed to increase the oxygen affinity of human haemoglobin and inhibit the sickling of sickle erythrocytes.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Antisickling Agents; Benzaldehydes; Diphosphoglyceric A | 1984 |
Impaired pentose phosphate shunt function in sickle cell disease: a potential mechanism for increased Heinz body formation and membrane lipid peroxidation.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Hemolytic; Anemia, Sickle Cell; Diphosphogly | 1983 |
Cryopreservation of cyanate-treated sickle erythrocytes.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Blood Preservation; Cyanates; D | 1982 |
Phosphorus-31 nuclear magnetic resonance studies of human red blood cells.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Anemia, Sickle Cell; Diphosphoglyceric Acids; Erythr | 1982 |
Sickling as a function of oxygen delivery: effect of simulated transfusions of stored, fresh and inositol-hexaphosphate-loaded (low affinity) red cells.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Diphosphoglyceric Acids; Erythrocytes, Abnormal; Exchan | 1982 |
Antisickling effects of 2,3-diphosphoglycerate depletion.
Topics: 2,3-Diphosphoglycerate; Adult; Anemia, Sickle Cell; Biopolymers; Cell Size; Diphosphoglyceric Acids; | 1995 |
Recombinant human hemoglobins designed for gene therapy of sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Amino Acid Sequence; Anemia, Sickle Cell; Animals; Base Sequence; Diphosphog | 1994 |
Intracellular hemoglobin S polymerization and the clinical severity of sickle cell anemia.
Topics: 2,3-Diphosphoglycerate; Adolescent; Adult; Anemia, Sickle Cell; Erythrocyte Indices; Erythrocytes; F | 1998 |
Second generation knockout sickle mice: the effect of HbF.
Topics: 2,3-Diphosphoglycerate; Age Factors; Anemia, Sickle Cell; Animals; Chromatography, High Pressure Liq | 2001 |
Deoxygenation permeabilizes sickle cell anaemia red cells to magnesium and reverses its gradient in the dense cells.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Biological Transport, Active; Cell Membrane Permeabilit | 1990 |
2,3-Diphosphoglycerate and intracellular pH as interdependent determinants of the physiologic solubility of deoxyhemoglobin S.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Adult; Analysis of Variance; Anemia, Sickle Cell; Di | 1990 |
Sickle cell disease in Sudan.
Topics: 2,3-Diphosphoglycerate; Adolescent; Adult; Anemia, Sickle Cell; Bilirubin; Child; Child, Preschool; | 1988 |
Arterial oxygen tension, haemoglobin F and red cell 2, 3 diphosphoglycerate in sickle cell anaemia patients with digital clubbing.
Topics: 2,3-Diphosphoglycerate; Adolescent; Anemia, Sickle Cell; Child; Child, Preschool; Diphosphoglyceric | 1989 |
Relationship between the nicotinamide adenine dinucleotide redox potential and the 2,3-diphosphoglycerate content in the erythrocyte in sickle cell disease.
Topics: 2,3-Diphosphoglycerate; Anemia, Hemolytic, Autoimmune; Anemia, Sickle Cell; Diphosphoglyceric Acids; | 1989 |
The effect of 2,3-diphosphoglycerate on the solubility of deoxyhemoglobin S.
Topics: 2,3-Diphosphoglycerate; Anemia, Sickle Cell; Binding Sites; Diphosphoglyceric Acids; Hemoglobin, Sic | 1986 |
[Protective effect of buflomedil hydrochloride on erythrocyte sickling. In vitro study].
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Adult; Anemia, Sickle Cell; Child; Child, Preschool; | 1986 |
Autologous survival of cyanate-treated cryopreserved sickle erythrocytes.
Topics: 2,3-Diphosphoglycerate; Adenosine Triphosphate; Adult; Anemia, Sickle Cell; Blood Preservation; Cyan | 1986 |