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Wise - CM 101

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    Wise - CM 101

    I did a search on cure for spinal cord injuries and found where the cancer drug cm101 was successful in recovering rats from spinal cord injury. This was in 1997. In the past 5 years since these results, what are the latest findings concerning CM101 ? Has there been human application or an understanding why the results were found with rats. Is this something your lab has collaborated with.

    I am not sure where CM101 is at the present. I know that the Vanderbilt group that did the original studies are still assessing the drug but I don't know other laboratories that are studying the drug. Wise.


      Bareback, it seems that CM101 minimizes inflammation and scarring in acute contusion injuries. Here are the latest post 1997 studies:

      Proc Natl Acad Sci U S A 1998 Oct 27;95(22):13188-93
      CM101-mediated recovery of walking ability in adult mice paralyzed by spinal cord injury.

      Wamil AW, Wamil BD, Hellerqvist CG.

      Department of Surgery, Vanderbilt University, Nashville, TN 37232, USA.

      CM101, an antiangiogenic polysaccharide derived from group B streptococcus, was administered by i.v. injection 1 hr post-spinal-cord crush injury in an effort to prevent inflammatory angiogenesis and gliosis (scarring) in a mouse model. We postulated that gliosis would sterically prevent the reestablishment of neuronal connectivity; thus, treatment with CM101 was repeated every other day for five more infusions for the purpose of facilitating regeneration of neuronal function. Twenty-five of 26 mice treated with CM101 survived 28 days after surgery, and 24 of 26 recovered walking ability within 2-12 days. Only 6 of 14 mice in the control groups survived 24 hr after spinal cord injury, and none recovered function in paralyzed limbs. MRI analysis of injured untreated and treated animals showed that CM101 reduced the area of damage at the site of spinal cord compression, which was corroborated by histological analysis of spinal cord sections from treated and control animals. Electrophysiologic measurements on isolated central nervous system and neurons in culture showed that CM101 protected axons from Wallerian degeneration; reversed gamma-aminobutyrate-mediated depolarization occurring in traumatized neurons; and improved recovery of neuronal conductivity of isolated central nervous system in culture.


      Angiogenesis 2001;4(1):61-70

      CM101 stimulates cutaneous wound healing through an anti-angiogenic mechanism.

      Nanney LB, Wamil BD, Whitsitt J, Cardwell NL, Davidson JM, Yan HP, Hellerqvist CG.

      Department of Plastic Surgery, Department of Cell Biology, Vanderbilt School of Medicine, Nashville, Tennessee, USA.

      CM101, an anti-pathoangiogenic polysaccharide derived from group B streptococcus, has been shown to inhibit inflammatory angiogenesis and accelerate wound healing in a mouse model and minimize scarring/gliosis following spinal cord injury. To evaluate the in vivo effects of CM101 on cutaneous wound healing in the pig, intravenously delivered CM101 or placebo vehicle was given 1 h after cutaneous wounding and again at 72 h after injury. Tissues from partial-thickness and full-thickness excisions were collected at days 4 and 7 after wounding and evaluated for a variety of standard healing parameters. Both types of CM101-treated wounds showed significantly less evidence of inflammatory angiogenesis when assessed by macroscopic photography of the wound surface, qualitative histological observations, laser doppler perfusion imaging, and quantitative morphometric analysis of microvessel area from endothelium selectively immunostained for factor VIII. Resurfacing was accelerated in partial-thickness and full-thickness excisions that received two doses of CM101 as compared to the placebo-treated excisional wounds. Neodermal thickness was increased in CM101-treated wounds at day 4 and was slightly reduced in comparison with placebo by day 7. New collagen accumulation appeared to be unaffected by the CM101 treatment. Immunohistochemical staining using a polyclonal antisera directed against the anti-pathoangiogenic CM101 target protein HP59 on day 7 indicated a strong immunoreactivity on the microvessels present in the control wounds but not in wounds of the CM101-treated animals. In summary, the immunolocalization HP59 in the microvessels of the cutaneous wound bed in control but not in CM101 treated wounds suggests that CM101 inhibits the pathologic inflammatory angiogenesis accompanying the normal granulation processes. The net biological effect of inhibited inflammatory pathoangiogenesis is a diminished, suggested and purely physiologic, microvascular bed which translates into an enhanced rate of epithelial resurfacing and therefore an overall accelerated rate of wound repair.