Phase I-II trial of Seraspenide (AcSDKP): a supressor of myelopoiesis protects against chemotherapy myelotoxicity (version 10 february 1993)

Carde, Patrice; Gonçalvès, Emanuel; Isnard, F; Paillette, E. Deschamps de; Chastang, Claude; Mathieu-Tubiana, N.; Vuillemin, E.; Delwail, Vincent; Corbion, O; Vekhoff, Anne; Ferrero, Jean Marc; García-Giralt, E; Gimonet, J.-F.; Stoppa, Anne‐Marie; Leger-Picherit, E.; Monpezat, J.-P.; Fadel, Élie; Domenge, C.; Guilhot, François; Thomas, François; Khayat, David; Monnier, Alain; Zittoun, R; Brun, Bernard; Maraninchi, D; Munck, Jean‐Nicolas; Beaujan, F; Guigon, Martine; Frindel, E; Najman, A; Tubiana, M

doi:10.1007/978-2-8178-0765-2_179

Cited by 6 publications

(9 citation statements)

References 7 publications

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“…5 and 12 . 5 mg kg ¹1 , to partially protect their haematopoiesis from the toxicity of chemotherapy [5].…”

Section: Discussionmentioning

confidence: 99%

“…These further modifications of blood progenitors could also be related to AcSDKP-induced alterations of the adhesion of bone marrow progenitors to their stromal environment. Alternatively, or concomitantly, they may be due to the wellknown in vitro and in vivo effects of AcSDKP on the cycling of haematopoietic progenitors in humans and mice [5][6][7]12].…”

Section: Discussionmentioning

confidence: 99%

“…It is produced by bone marrow stromal cells [2] and its concentrations in tissues and plasma vary in disease states and during chemotherapy [3,4]. Injection of synthetic AcSDKP (Goralatide) reduces the haematological cytopenia induced by chemotherapy in cancer patients [5] and protects haematopoietic progenitors in mice treated with cytotoxic drugs [6,7].…”

Section: Introductionmentioning

confidence: 99%

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Effects of the angiotensin‐converting enzyme inhibitor enalapril on blood haematopoietic progenitors and Acetyl‐N‐Ser‐Asp‐Lys‐Pro concentrations

Comte¹,

Lorgeot²,

Volkov³

et al. 1997

Eur J Clin Investigation

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Acetyl-N-Ser-Asp-Lys-Pro (AcSDKP) is a physiological inhibitor of the proliferation of haematopoietic stem cells. In 12 healthy volunteers treated with the angiotensin-converting enzyme (ACE) inhibitor enalapril (20 mg day-1 for 15 days), we studied plasma and urinary AcSDKP levels, the in vitro degradation of AcSDKP by plasma ACE and the numbers of circulating haematopoietic progenitors (granulocyte-monocytic colony forming unit: CFU-GM; burst forming unit-erythroid: BFU-E; and mixed colony forming unit: CFU-mixed). During treatment, plasma and urinary AcSDKP concentrations increased 2- to 5-fold, degradation of AcSDKP was reduced, and CFU-mixed significantly increased by 100% while BFU-E and CFU-GM significantly decreased by 16% and 26%, respectively. These results indicate that ACE inhibitors may be of value during chemotherapy or radiotherapy, warranting further study.

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“…5 and 12 . 5 mg kg ¹1 , to partially protect their haematopoiesis from the toxicity of chemotherapy [5].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of the angiotensin‐converting enzyme inhibitor enalapril on blood haematopoietic progenitors and Acetyl‐N‐Ser‐Asp‐Lys‐Pro concentrations

Comte¹,

Lorgeot²,

Volkov³

et al. 1997

Eur J Clin Investigation

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“…Moreover, MIP-la is not the only inhibitor of primitive normal progenitor cycling to display this lack of effect on primitive CML cells. Analogous in vitro studies with the tetrapeptide, AcSDKP, indicate that this molecule, already being tested in a phase I toxicity trial [50], may parallel MIP-1 a in its effects on primitive normal and CML progenitors [40].…”

Section: Properties Of Normal and CML Stem Cells That May Be Useful Fmentioning

confidence: 99%

Biological strategies for the selective manipulation of normal and leukemic stem cells

Eaves¹,

Cashman²,

Zoumbos³

et al. 1993

Stem Cells

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Abstract. Recent developments have occurred in the identification and quantitation of a very primitive type of hematopoietic cell (referred to as a long-term culture initiating cell or LTC-IC) using defined long-term culture conditions. These have facilitated investigations of the numbers and prop erties of both normal and leukemic LTC-IC in patients with chronic myeloid leukemia (CML). Such studies have revealed that the marrow of many chronic phase patients contains a substantlsl population of normal LTC-IC that are lunctionally intact albeit suppressed in vivo. Leukemic LTC-IC are typically less numerous in the marrow of these patients but are found in elevated numbers in the peripheral blood which, on average, in total contains more leukemic LTC-IC than the marrow when the WBC count rises above 10" per liter. However, a very marked heterogeneity in all of these parameters exists among individual patients. Some of the properties of leukemic LTC-IC are indistinguishable from those of their normal counterparts. Others, particularly those typically assodated with an activated state, are altered, although frequently in only 90% (or less) of the leukemic LTC-IC. A more marked disparity between primitive normal and leukemic LTC-IC is seen in terms of their relative abilities to maintain their numbers in vitro. At the level of primitive donogenic cells, the leukemic population has heen shown to exhibit an increased rate of turnover. This appears to be due to an inability of these cells to respond to the cytostatic effects of macrophage inflammatory protein-la --la).Tbese findingy provide new insights into the biology of CML and highlight the power of quantitative assays to guide the development of more generally applicable curative therapies.

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“…These properties of AcSDKP suggest its possible clinical use for protection of haematopoiesis during chemo-and radiotherapy. The results of the first clinical trials have already shown that the administration of synthetic AcSDKP (Goralatide) in association with a chemotherapeutic regimen in cancer patients reduces the period of neutropenia [12]. The endogenous level of AcSDKP is regulated by a complex balance between its de novo synthesis by living cells, its release from damaged cells, its catabolism and urinary elimination.…”

Section: Introductionmentioning

confidence: 99%

In vivo modifications of AcSDKP metabolism and haematopoiesis in mice treated with 5‐fluorouracil and Goralatide

Comte¹,

Lorgeot²,

Bignon

et al. 1998

Eur J Clin Investigation

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Phase I-II trial of Seraspenide (AcSDKP): a supressor of myelopoiesis protects against chemotherapy myelotoxicity (version 10 february 1993)

Cited by 6 publications

References 7 publications

Effects of the angiotensin‐converting enzyme inhibitor enalapril on blood haematopoietic progenitors and Acetyl‐N‐Ser‐Asp‐Lys‐Pro concentrations

Effects of the angiotensin‐converting enzyme inhibitor enalapril on blood haematopoietic progenitors and Acetyl‐N‐Ser‐Asp‐Lys‐Pro concentrations

Biological strategies for the selective manipulation of normal and leukemic stem cells

In vivo modifications of AcSDKP metabolism and haematopoiesis in mice treated with 5‐fluorouracil and Goralatide

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